text:
Arizona authorities are trying to identify possible victims of illegal cosmetic surgery procedures performed in the Tucson area.
That word comes from the Attorney General's Office in the wake of the arrest of a Tucson man who is accused of performing fat-removing liposuctions illegally out of his home.
The office says 51-year-old Gustavo Felix Nunez is not a physician and is not licensed in Arizona to practice medicine.
The office says authorities are seeking people who have undergone cosmetic surgery at Nunez's home on the 8600 block of North Bobby Jones Drive, at an industrial warehouse located at 1656 N. 15th Ave. or other locations.
According to the office, the procedures could include liposuctions, lip injections, Botox injections, and other similar cosmetic procedures and plastic surgeries.
Copyright 2014 Associated Press. All rights reserved.


text:
Technical ProblemsIf you can't download lecture notes or have problems with watching lectures please visit the support page>>
If you find OpenTuition study materials useful in your studies, please consider making a donation - it will help us enormously to be able to expand and improve the resources that we offer.Donate here
Samphos says
Are there lecture for the following Chapters?
– Chapter 15: Mergers and acquisitions
– Chapter 16: The valuation of acquisitions and mergers
– Chapter 17: Corporate reorganization and capital reconstruction schemes
Thank you!
John Moffat says
Chapter 15 is purely written and does not warrant a lecture – it is for you to read yourself.
Chapter 16 has involves no techniques that have to already been covered in earlier chapters. The problem is one of approach to the question and for this reason I have recorded several lectures working through a few past Question 1's from the exam, where I discuss the approach as well as obviously work through the technical aspects.
Chapter 17 is really a financial accounts topic (even though it is asked from time to time in P4) and is therefore revision from P2.
Samphos says
Thank you very much!
John Moffat says
You are welcome 🙂
babybupe says
I can't see chapter 15 and 16 for mergers and acquitions. where are they?
John Moffat says
Please ask this sort of question in the P4 Ask the Tutor Forum and not as a comment on a lecture on something different.
shafqaat says
To make it easier to remember, try reading $/£ as $ per £. E.g. If the $/£ rate is 0.77 read it like $ per £ is 0.77, per £ means one Pound.
Leanne says
Hi John
I am loving your lectures thank you. I am wondering however will I cover enough material with these lectures and the BPP revision kit or should I be using the BPP study text also?
Thanks 🙂
John Moffat says
The lectures cover everything you need to be able to pass the exam well.
You need to practice lots of questions and your Revision Kit is fine for that.
You do not really need to use the Study Text. Best is to use it if there is anything you are not clear about in the lectures or if you have time for extra reading.
And please in future ask questions in the Ask the Tutor Forum rather than as a comment on a lecture 🙂
kaynat says
Hello Sir, I am very pleased that I found your lectures. These Forex rates always confuse me, unfortunately thats my third attempt at p4 , while I passed all papers at first attempt, so I am so much worried but I hope now I gain plenty of good marks in march attempt.
Thank u very very much Sir,,,
John Moffat says
You are welcome, and good luck 🙂
tah3000 says
This is different from how currency pairs are quoted in real life though. EURUSD = 1.1000 means 1 euro (the base currency) is equivalent to $1.10 (the quote or counter currency).
John Moffat says
In depends which country you are in – some countries quote one way and some countries quote a different way. There is no 'world-wide' rule.
The exam always makes it clear which way round the quote is given.
fahim231 says
Hello sir can you please help me with the following – are forward rate agreements the same as future contracts? and what does it mean when it is quoted like this 6V9 – 7•30 – 7.00%
John Moffat says
No – FRA's are not the same as futures.
You have asked this below a lecture on foreign exchange risk management, whereas FRA's relate to interest rate risk management (and are dealt with in those lectures!).
It is where the bank will fix an interest rate today for a loan or deposit starting on a future date.
In your example, it means that for a loan starting in 6 months time and finishing in 9 months time (i.e. a 3 month loan) they offer fixed interest of 7.00% per year on deposits and charge interest of 7.30% on loans.
fahim231 says
Ok thank you
sogan0 says
Okay here is another silly question well there isnt right. We in UK we need to receive $ therefore inorder for us to receive $ im in the bank what do i do sell or buy pounds? On the other hand if we need to pay$ we need to buy $ therefore we have to sell pounds in order to buy $. What is the rule here? Im imagining myself at the bank to pay $ and what i would do over the counter in the bank.
John Moffat says
If you receive $'s from a customer, then you will sell the $'s to the bank and receive £'s from the bank (same a buying £'s from the bank and paying for them in $'s)
sogan0 says
so if you need to pay $ then u buy pounds from the bank?
John Moffat says
No – why would you want to buy GBP's if you are in the UK and need to pay $'s??
If you need to pay $'s then you will buy $'s from the bank which means selling GBP's to the bank.
sogan0 says
really is that it?
John Moffat says
Is what it ???
sogan0 says
whether u need to multiply if u use first currency and divide if using second currency
sogan0 says
Hi I still get confused when to multiply or when to divide i know which exchange rate to use but not sure whther to divide or sell
Am i right by saying if you need to calculate the first currency you multiply and if you need to calculate the second currency you divide?
John Moffat says
That's correct 🙂
harryamoatey says
the is no video for the p4 note. it seems it has been taken down
John Moffat says
The video has not been taken down and is working fine.
Any problem must be at your end – you should visit the support page (the link is above).
OLAYEMI says
I want to specially thank you for the video lectures uploaded. But at the same time, I will like you to give instructions on downloading these video lectures so that one can watch them over and over again even when there is no internet access.
John Moffat says
The lectures can only be watched online – they cannot be downloaded.
This is the only way that we can keep this website free of charge.
iresha2sanjeevani says
Thanks a lot opentution…..nw only i got it right. all these times it was confusing me n now i got d correct logic. Thanks again….
karmuks says
I am sorry if do not understand something. But in example after example 1 the second example where we sell GBP 1,493,250.00 and get for it only Euro 500,000.00? Please explain if I am missing something.
John Moffat says
I am not sure what the problem you are having is.
The exchange rate given is £/Eur 2.9865
This means that 2.9865 £'s are equal to 1 EUR. The way rates are quoted in the exam is that 2.9865 of the first quoted currency (here £'s) = 1 of the second quoted currency (here Euros).
So 2 EUR = 2 x 2.9865 £'s and so on.
So 500,000 EUR = 500,000 x 2.9865 £'s = GBP 1493250
What might be confusing you is that often on the TV etc, they quote rates differently, but the rule in the exam is that above.
Also, of course the rate I have given is not realistic (at the moment!) but in the exam obviously you use whatever rate you are given.
karmuks says
The way showed how to calculate exchange for me seems correct and understandable. What confuses me is that 1 euro is worth more than 1 pound. Or I should not pay attention to it?
John Moffat says
As I said in my previous reply, the exchange rate used is nothing like the current exchange rate. However in the exam you use whatever exchange rate is given to you.
(At present 1 Euro is worth less than 1 pound, but that might not always be the case, and there are certainly other currencies that are worth more than 1 pound.)
deepmaharaj says
Very nice lecture. God bless.
hssniqbl says
I think the easy way to remember is to think that we will always be at loss. So we choose the rate which costs us more or gives us less.. Is this okay?
John Moffat says
That's fine. As long as you can get the correct rate to use quickly, then whatever way is easiest for you 🙂
garygood says
Sorry I forgot to add that usually all currencies are quoted against USD except the "Queen's curriencies" i.e. GBP, AUSD, NZD etc. and also the Euro that are quoted as base currencies therefore instead of $/£ (as shown in the example) we would have GBPUSD (£/$) pair – therefore it would correctly be 1.6 USD for every 1 GBP.
I think. But I could be wrong.
John Moffat says
Which way round currencies are quoted differs between countries, and also between channels (e.g. the way the bank quotes is not necessarily the same way round as the way TV channels quote).
What is in the lecture is correct for the exam!
See my other answer below.
garygood says
I agree. Many thanks.
garygood says
I've read everywhere else that the currency quotes are always: 1 of base currency (i.e. $ in this case) to however much of the counter currency (i.e £1.6 in the above example). Here the lecturer says it is the other way around.
Forgive me but am I missing something?
John Moffat says
The lecture makes it clear and is correct.
In practice there are always 2 ways of quoting exchange rates – there is no 'official' way of quoting them (even though most quote against their own currency.
However in the exam, if it is (for example) a $/£ quote, then it is giving the number of $'s that equal 1 £
Similarly if it is a EUR/$ quote, then it is giving the number of EUR that equal 1 $
I am only concerned about helping people to pass the exam, and in the exam the quotes are always as above (and as per the lecture) unless, obviously, you are told different.
garygood says
Many thanks Mr Moffat. It can get confusing at times (at least for me, it does), but your explanations are very clear, as always. I'll stick with your method. Cheers!
John Moffat says
I agree that it is confusing (and thank you for the comments) 🙂
ocys says
this video might just do the trick to finally understand foreign exchange
baygaliya says
thank you for the lecture, so easy to understand and to apply the knowledge
ignatius001 says
Awesome, I now totally understand it. I used to mix up the buying and selling rates between the bank and customer. It has been ironed out. Thanks O.T
nailya1908 says
Wowww Thank you so much for your work!!
nengibob says
Really nice. definitely got it now.
waleedpecian says
This is a great lecture. I am now very much clear about the concept of buyinh and selling rates and how to use them…
simelanempumie says
Thanks for the tips. It is clearer now. Great Lecture
kerry says
Now the home,base and cross currency that I have learnt is much clearer. Until this I couldn't get it right. Thanks
timg says
You really only get the beauty of this presentation when you have had to reverse engineer how some of the text books present this…
zaneta says
These letures on Chapter 17 are great! I watched all of them and they helped me enormously, so a HUGE thank you to Open Tuition!!!
mwachilale says
You have ironed out the common errors that I have been making when converting the currencies.
oseidarko says
Wow! What can I say? I just love it.
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subset: commoncrawl


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This year's shark week just ended, but why not dredge up another cool shark story? Marine biologists from Stanford University found an unlikely surfer to help them track the migration routes of Great White Sharks: the Wave Glider robot. What will those brainy Stanford Trees think of next?!


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Posted by R. Berg on November 30, 2003
In Reply to: Concord: do or does posted by Henry on November 30, 2003
: : Just now I was reading the liner notes to the Chet Baker CD called simply "Chet". It says: "Although this album is entirely devoted to explorations of the ballad mood, it includes considerable variety. Approach, instrumentation, even tempo does not remain constant here." I'm interested in the second sentence; the first is included merely for the sake of providing context. It sounds all right, so it may not strike you as odd; indeed, I believe it is grammatically in order. However, consider this sentence, which, as it were, lurks in the background: "Approach, instrumentation, AND tempo DO not remain constant here." That is, I've taken out "even" and inserted "and." Now, clearly "does" becomes "do." So, why is "does" correct in the original sentence (and "do" wrong)? I suppose because of "even," which is associated with "tempo." Try to replace "does" with "do" in the original sentence - clearly, this is wrong! We are told that tempo does not remain constant, but there seems to be a verb lacking for "approach" and "instrumentation." That is, when speaking in terms of concord, indeed, the verb is lacking; but, in terms of meaning, the two nouns "borrow" from "does." This is why the "and . . . do" sentence lurks in the background. I don't know what grammarians call this structure. Your comments will be much appreciated. Thanks.
: : Anders
: There's an omission in the original phrase. We don't know if the writer is referring to each of the items or all of them. It could be amended in a number of ways. It might have been written;
: Approach, instrumentation, even tempo; each does not remain constant here.
: or;
: Approach, instrumentation, even tempo; all do not remain constant here.
: It could be rewritten as you suggest;
: Approach, instrumentation and even tempo do not remain constant here.
: The use of 'do' in the original doesn't sound obviously wrong to my ears;
: Approach, instrumentation, even tempo do not remain constant here.
Anders, how do you know that the word to insert in the original sentence is "and," not "or"? "Or" fits the meaning in a subtly better way than "and," considering that the word "even" is there. The three elements (tempo...) are being considered one at a time.


text:
Boxing matches/fighters that belong on a network like Fox?
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I personally hate the term "tv friendly" fighter asthat translates loosely into, "slugger, no defense, limited skills, can either knockout or be knocked out".
I do think you make a point though but I think part of the problem is this. Boxing is one of the FEW sports (and I'm speaking from the US/Stateside of things) where you really can't follow rise of a fighter casually. I think even if you're a hard-core fan you can't follow the rise of guys because a lot of amateur stuff isn't televised.
That said, I think what happens is the average viewing fan doesn't know how to recognize or appreciate a skilled boxer. IMO you have these levels of fighters.
- These are guys who not only aren't in shape but probably were picked up from the latest tough man contest. Examples.. None other than KIMBO Slice and the guy who he was fighting.
- They understand how to pace themselves, can throw most punches and they do actually train. They can be entertaining and if they're more active or have punching power, they "CAN" beat a guy with a higher skill level.. Examples..
- This is a wide category and a lot of boxers fall in here. These are guys who do one thing good but may have other holes. These are also guys may have been "very good" or are vets that are now shop worn. Examples are "Gatekeeper guys (Zab Judah, Vivian Harris, Chop Chop Corley), Pavlik, etc...
Very Good
- IMO these are the guys STRICTLY that should be on the premium networks. These are guys who do MULTIPLE things good.
- IMO there's less than 10 of these in the sport. These are guys who not only do multiple things good, they do them EXCELLENT. They also have the ability to make a "Very Good" fighter look like a "good" or "fair" fighter.
Examples.. Money, Pac, Martinez, Klitchko, Donaire, Hopkins, Ward, etc.
If more casual fans KNEW how to grade fighters, the networks would know how to match up or choose fighters. Frankly more often than not, a lot of match-making deals more with how a fighter "draws".
I will say this though, ESPN's FRIDAY night FIGHTS this year has been more entertaining than HBOs fights.
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text:
Federal regulators investigating the accounting of embattled Fannie Mae have discovered additional serious problems.
WASHINGTON — Federal regulators investigating the accounting of embattled Fannie Mae have discovered additional serious problems, the mortgage giant disclosed yesterday, as it received a three-month extension for boosting its capital cushion against risk.
The biggest U.S. buyer of home mortgages has been reducing its portfolio of home loans even faster than expected as it prepared to meet the regulators' original June deadline for a $5 billion capital boost.
An eight-month investigation by the Office of Federal Housing Enterprise Oversight (OFHEO), which supervises Fannie Mae, last year found serious accounting problems at the government-sponsored company as well as a pervasive pattern of earnings manipulation and lax internal controls. The Securities and Exchange Commission ordered Fannie Mae in December to restate its earnings back to 2001, a correction estimated at $9 billion. The company's chief executive, Franklin Raines, and chief financial officer, Timothy Howard, were forced out by the board of directors.
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Now OFHEO, whose examination continues, has informed Fannie Mae's board of additional problems including accounting for securities and loans, and practices to spread the impact of income and expenses over time, the company said in a statement. It said the agency had identified internal-control deficiencies at the company "that it believes raise safety and soundness concerns."
Fannie Mae shares, which have been battered in the weeks since its accounting crisis came to light on Sept. 22, fell 64 cents to close at $57.16, their lowest level in more than four years and 30 percent below their high of $80.82 a year ago.
"We're getting a broader, more detailed understanding of the specific accounting issues, but I don't see this as anything new," said Bert Ely, a banking consultant in Alexandria, Va., and longtime critic of Fannie Mae.
In its statement, the company said its board and management "are addressing the issues and questions."
"Fannie Mae will report to OFHEO regarding each of these issues, and will continue to work with OFHEO to resolve these matters as part of the company's ongoing internal reviews and its restatement process," it said.
In September, the regulators ordered Fannie Mae to boost its capital cushion against risk by 30 percent, or some $5 billion, by the middle of this year.
The company said yesterday that the agency had extended that deadline until Sept. 30.
OFHEO spokeswoman Corinne Russell declined comment.
Washington-based Fannie Mae has been shrinking its loan portfolio even faster than expected as it prepared to meet the original June deadline. Its spectacular growth of recent years could be curtailed.
The company said Monday that its gross portfolio, which includes both its own investments and mortgage-backed securities it guarantees that are held by other investors, fell to $890 billion at the end of January from $904.6 billion in December, for an annualized rate of decline of 16.8 percent.
By comparison, Fannie Mae's mortgage portfolio fell at an annualized rate of 10.1 percent in December, bringing growth for 2004 as a whole to 0.7 percent, compared with 2003's 13.1 percent pace.
In recent weeks the company also has raised fresh capital by issuing some $5 billion in preferred stock and slashed its first-quarter dividend payout by half, to 26 cents a share, to make up its anticipated shortfall.
To cut costs, Fannie Mae last month stopped awarding stock options to senior managers. As further cost-cutting measures, the politically influential company disclosed yesterday that it will "sharply curtail its corporate advertising campaign and use of political consultants."
Fannie Mae and Freddie Mac, its smaller rival in the $8 trillion home-mortgage market, have wielded influence in Congress and traditionally have been heavy contributors to lawmakers of both parties. The accounting crisis at Fannie Mae, and Freddie Mac's disclosure in June 2003 that it had understated profits by some $4.5 billion for 2000-2002 in an effort to smooth earnings, have bolstered calls by lawmakers and government officials for tighter regulation of the two and curtailment of their privileges.
On Tuesday, OFHEO said it had proposed requiring Fannie Mae and Freddie Mac to promptly report mortgage fraud or suspected fraud to the government and to establish internal controls to detect it. The action followed the alleged defrauding of U.S. housing finance agency Ginnie Mae.
In addition, OFHEO Director Armando Falcon ordered Fannie Mae and Freddie Mac to notify the agency of any government investigations or civil or criminal actions, or lawsuits by private parties such as shareholders.
The two companies, created by Congress, pump money into the home-mortgage market by buying and guaranteeing repayment of billions of dollars of home loans each year from banks and other lenders, then bundling them into securities that are resold to investors worldwide.


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THIS RESTAURANT IS CLOSED Five Points
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By Patrick Meskell
Fifty by fifty. That is… run an ultramarathon, specifically a 50 mile race, by age 50. It sounds simple enough, and at age 47, I actually have more than one year to get it done. But I figure that I better give myself a little room for setbacks such as illness or injury. As New Year's resolutions go, it's not going to change the world, but is certainly one of the tougher goals that I have personally made.
"Ultrarunning" as a sport is still in its infancy, but is growing in the collective consciousness of runners at a very rapid pace. An ultramarathon, or "ultra," is any running event that is longer than a marathon, usually 50K, 50 miles, 100K, or 100 miles. However, this column is not meant to be sage advice from an expert, but more of a trial and error, "don't-make-the-same-mistake-that-I-just-did," how-to (or how-not-to) train for an ultra. In other words, "A Beginner's Guide" means "by a beginner" more than it means "for beginners."
Each week I will try to cover different aspects of running, using my own training schedule and progress, most of which will apply to running of any distance, but some of which will be specific to running ultras. For example, getting lost during a race… in the middle of the night… on a badly marked trail… lit only by a tiny handheld flashlight… and the nearest runner to you is over a half hour ahead or behind. I haven't yet experienced this particular thrill, but apparently it's quite common in the longer races.
Sunday, Feb. 12, I ran in the San Dieguito Half Marathon. I was one of three runners from Ramona out of about 1,300 participants. (A shout-out to my fellow Ramonans — L. Robison and S. Monreal!) San Dieguito is a nice course, though not particularly easy as it winds the 13.1 miles over rolling hills in Del Mar. My goal was to run smoothly, and treat it as a training run, carrying two water bottles with me (a hand-held and one on a waist pack), since aid stations on many of the longer runs are often five to 10 miles apart. I finished in 1:50:50 (1 hour, 50 minutes, 50 seconds), a pace of 8:28 per mile. That's probably much too fast a pace for me in an ultra, but we'll see. I was a little sore the next day, but nothing too severe.
Hopefully anyone interested in running, no matter what age or level of runner you are (and admittedly many readers will be far more advanced runners than I), will find this column interesting and somewhat educational. And hopefully I will run and finish the 50-miler a lot sooner than age 50, but it's hard to know what to expect at this point. Besides, "50 by 49" just doesn't have the same ring to it.
Now get out and run.


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What is a Trust?
The concept of a Trust is over 900 years old and originates from English Law. Over time the South African Law on Trusts has been developed by the legislature, the courts and legal practitioners into what we find today.
A Trust is a separate legal entity but not a legal persona or a juristic person per se. A Trust is created by a contract called a Trust deed which is entered into by certain parties.
A Trust can be described as a legal relationship created by a person (known as the Founder), by placing assets under control of another person (known as the Trustee), during the Founders lifetime (known as an Inter Vivos Trust) or on the Founder's death (known as a Testamentary Trust) for the benefit of third parties (the Beneficiaries).
Parties to a Trust
The parties to a Trust are the Founder, the Trustees, and the Beneficiaries.
Founder/ Settlor
The Founder is the person who creates the Trust and makes the initial funds available to the Trust and is also known as the "Donor" or "Settlor". The Founder should be of majority age.
Contrary to popular belief the same person can be the Founder, Trustee and Beneficiary of a Trust, on the condition that the Trust deed is correctly structured.
The Trustees are appointed in the Trust deed and are charged with the administration of the Trust. They must comply with the Trust Property Control Act and act in accordance with the Trust deed.
A Trustee may only act on behalf of the Trust once they have received the Letters of Authority that are issued by the Master of the High Court.
Choosing the Trustees is very important. The Trustees must be persons of integrity, someone that will act with care, diligence and skill reasonably expected of a person who manages the affairs of another. A Trustee should be someone who owes the utmost good faith towards the Beneficiaries in carrying out the obligations imposed upon them by the Trust Deed.
Independent Trustees
It is very important that the Board of Trustees has a certain degree of independence and not be mere agents of the Beneficiaries or Founder.
An Independent Trustee is some-one who is not related to and arms length to the Beneficiaries. This person (or entity) should be some-one who has the necessary legal, tax and trust administration knowledge to ensure the correct administration of the Trust.
Appointing an Independent Trustee will ensure that there is indeed a clear distinction between control and enjoyment of the Trust assets, thereby protecting the integrity and efficiency of the Trust as a separate entity.
The Independent Trustee will also ensure impartiality in decisions that need be made on behalf of the Trust and can act as a mediator in the event of disputes.
Any person can be a Beneficiary of the Trust. In most instances, the Beneficiaries would be the persons that you would normally nominate to benefit from your estate in your Will.
There is also no limit to the number of Beneficiaries to the Trust. Persons other than natural persons can also be Beneficiaries such as, duly registered Trusts, juristic persons, associations, to name but a few.
It is advisable that the Beneficiaries should be discretionary Beneficiaries to the income and capital of the Trust. In such a case, the Beneficiaries shall have no rights whatsoever to claim Trust benefits as and when they please. This will also result in the assets being secure from the creditors of the Beneficiaries and cannot be taken into account as part of their estate on death.


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Adenosine is an ATP breakdown product that in most vessels causes vasodilatation and that contributes to the metabolic control of organ perfusion, i.e., to the match between oxygen demand and oxygen delivery. In the renal vasculature, in contrast, adenosine can produce vasoconstriction, a response that has been suggested to be an organ-specific version of metabolic control designed to restrict organ perfusion when transport work increases. However, the vasoconstriction elicited by an intravenous infusion of adenosine is only short lasting, being replaced within 1–2 min by vasodilatation. It appears that the steady-state response to the increase of plasma adenosine levels above normal resulting from the infusion is global renal vasorelaxation that is the result of A2AR activation in most parts of the renal vasculature, including larger renal arteries, juxtamedullary afferent arterioles, efferent arterioles, and medullary vessels. A2AR-mediated vasorelaxation is probably facilitated by endothelial receptors that cause the release of nitric oxide and other endothelial relaxing factors. In contrast, isolated perfused afferent arterioles of superficial and midcortical nephrons of rabbit and mouse, especially in their most distal segment at the entrance to the glomerulus, respond to adenosine with persistent vasoconstriction, indicating predominant or exclusive expression of A1AR. A1AR in afferent arterioles are selectively activated from the interstitial aspect of the vessel. This property can dissociate A1AR activation from changes in vascular adenosine concentration, a characteristic that is ideally suited for the role of renal adenosine as a paracrine factor in the control of glomerular function.
- adenosine receptors
- vascular resistance
- renal blood flow
- endothelium
the extracellular actions of adenosine are mediated by binding of the nucleoside to four types of G protein-coupled membrane receptors, A1, A2a, A2b, and A3 adenosine receptors (A1AR, A2aAR, A2bAR, A3AR). The expression pattern of adenosine receptor subtypes throughout the organism is extremely widespread, commensurate with the organismwide actions of the nucleoside. In most blood vessels, adenosine elicits marked vasodilatation, and this effect is mediated by A2aAR and A2bAR, G protein-coupled receptors that induce relaxation through the Gsα and protein kinase A pathway. Adenosine-induced vasodilatation reflects dominance of A2AR in the vasculature of most tissues and organs. In contrast, A1AR coupled to Giα and PLC activate motor activity of smooth muscle cells in a number of muscular tissues (4, 44, 65, 67), but this receptor subtype is not widely expressed in the vasculature. A1AR are, however, present in blood vessels of the kidney besides A2AR, and this has made the renal vascular actions of adenosine comparatively complex.
Evidence obtained in the 1960s solidified an earlier observation that the kidney vasculature differs from other vascular beds in that the overall effect of exogenous adenosine may be vasoconstriction (17, 24, 81). This remarkable observation of a constrictor effect exerted by a prototypical metabolic dilator has been the focus of numerous discussions, but its understanding is still incomplete. A renewed interest in the vasoconstrictor action of adenosine has resulted from the recent evidence in support of the notion that the nucleoside is responsible for the afferent arteriolar constriction caused by increasing NaCl concentration at the macula densa, the so-called tubuloglomerular feedback (TGF) response (10, 76, 80). Although the vasoconstrictor potential of adenosine at the organ level has been the origin of the proposal of adenosine acting as the constrictor mediator of the TGF response (55), this reasoning has always been weakened by an apparent, but not fully acknowledged, internal inconsistency. The main problem has been that the vasoconstriction and the accompanying decrease in renal blood flow at the organ level are only a transient phenomenon, whereas the steady-state effect of adenosine is either no change or an increase in renal blood flow (23, 52, 54, 74, 77). Thus the temporal characteristics of the effects of changes in adenosine levels on global renal vasoconstriction and on TGF-induced vasoconstriction are apparently entirely different, making it difficult to accept that these responses are mediated by the same receptors (51). Because the kidney vasculature is sufficiently heterogeneous, it has been common to argue that adenosine causes vasoconstriction in one part of the renal vascular bed and vasodilatation in another, for example, that afferent arteriolar vasoconstriction is accompanied and overcome by efferent vasodilatation (77) or that superficial vasoconstriction is accompanied and overcome by juxtamedullary vasodilatation (58).
In the present review, we make an attempt to reconcile the failure of adenosine to cause a lasting global renal vasoconstriction with its ability to markedly and persistently elicit vasoconstriction at the arteriolar level, both pharmacologically and in its presumed physiological equivalent, the TGF response. Our overall conclusion is that the dominant effect of exogenous adenosine in the whole kidney is vasodilatation, which like in other vascular beds is a reflection of the wide distribution of A2AR in the renal vasculature and their activation by the supranormal adenosine levels resulting from the infusion. However, the distal afferent arteriole at the entrance to the glomerulus constricts to adenosine over a much wider concentration range than any other vascular segment, perhaps reflecting predominant or exclusive expression of A1AR. Because the region of A1AR-mediated vasoconstriction at high adenosine concentrations is restricted to a narrow segment, the effect of A1AR activation on total renal vascular resistance can be overcome when adenosine levels exceed normal concentrations and A2bAR in other parts of the renal vasculature are fully engaged.
The scarcity of reliable antibodies and radiolabeling probes and the low expression levels have made it unexpectedly difficult to precisely identify the adenosine receptor subtypes present along the renal vasculature. Global expression in rat renal cortical and medullary tissue has been shown for all four adenosine receptors at both the mRNA and protein levels (29, 40, 93). Studies in a preglomerular vessel preparation containing arcuate and interlobular arteries as well as afferent arterioles have identified the presence of A1AR protein and mRNA, but this approach does not resolve the expression profile along the longitudinal axis of the preglomerular vasculature (29). By in situ hybridization, cortical A1AR mRNA was found exclusively at the glomerular vascular pole but not over the glomerulus itself (83). Although it is unclear whether the signal originated in granular, extraglomerular mesangial, or vascular smooth muscle cells, one may conclude that some cells at the glomerular vascular pole express A1AR at much higher levels than any other vessel. RT-PCR assessment of A1AR mRNA expression has confirmed its presence in dissected glomeruli (88). More recently, immunohistochemical evidence has suggested the presence of A1AR expression in glomerular vessels, presumably in afferent arterioles, and inside the glomerulum, presumably in mesangial cells (71). However, of two antibodies directed against different epitopes, only one showed positive staining, an observation that cautions against overinterpretation of antibody-based evidence. In regard to A2 receptors, it has been reported that preglomerular vessels express only the low-affinity A2bAR at high levels but not the high-affinity A2aAR receptor protein (29). In situ hybridization failed to detect either A2aAR or A2bAR mRNA in the renal cortex (83). The profile of adenosine receptor expression in efferent arterioles has not been determined with any degree of certainty. In outer medullary descending vasa recta, RT-PCR analysis revealed expression of A1AR, A2aAR, and A2bAR, which was verified by Southern blotting (33). Receptor-binding studies using the well-defined panel of stable and selective ligands for adenosine receptor subtypes have not been performed in renal vascular tissue. In conclusion, the functional clues that can be derived from expression studies are relatively limited, but it seems clear that A1AR are predominantly expressed in afferent arterioles. A2AR, mostly A2bAR, are present in all preglomerular vessels and in descending vasa recta. No reliable information is available for efferent arterioles.
Effect of Adenosine at the Organ Level
There is abundant evidence to show that bolus injections of adenosine cause an immediate reduction in renal blood flow reflecting the response to activation of high-affinity A1AR (24, 56, 77, 81). Because this blood flow response was seen when adenosine was injected in the renal artery, it is not mediated by systemic consequences of adenosine such as a reduction in blood pressure (24, 54). A reduction in renal blood flow was also observed during continuous administration of adenosine, but this decrease was only short lasting and waned within 1–2 min. The transient constrictor effect was blocked by nonspecific and A1AR-specific antagonists, and it is absent in A1AR knockout mice, indicating that it is mediated by activation of A1AR (3, 54). This is supported by the persistent reduction in renal blood flow and glomerular filtration rate (GFR) induced by the infusion of the A1AR-specific agonist cyclohexyladenosine (CHA; see Ref. 13). In the isolated perfused kidney, CHA causes increasing vasoconstriction in the dose range between 10–9 and 10–7 M, whereas concentrations >10–6 M cause vasodilatation no doubt because of spillover onto A2AR with undefined vascular localization (43, 46). On the basis of hemodynamic modeling, the reduction in renal blood flow was attributed to a preglomerular, presumably afferent, arteriolar vasoconstriction (43, 77). The administration of A1AR antagonists does not usually cause major increases in renal blood flow, suggesting either that A1AR activation does not contribute to renal vascular resistance under resting conditions or that the effect of the inhibitors is incomplete (3, 34). GFR, on the other hand, is typically increased by A1AR antagonists (5, 41, 86).
Effect of Adenosine in Glomerular Arterioles
Superficial afferent arterioles. Micropuncture studies in dogs have shown that an intrarenal adenosine infusion caused a doubling of preglomerular arteriolar resistance (58). In rats, adenosine caused a fall in glomerular capillary and welling point pressures and a fall in superficial nephron GFR (SNGFR), results consistent with preglomerular arteriolar vasoconstriction (22). In contrast to the transient reduction in renal blood flow, the effects of adenosine on SNGFR were persistent. Thus the constrictor response in superficial nephrons occurs in the absence of changes in renal plasma flow and with only small or no changes in kidney GFR (57, 58). These observations appear to be internally inconsistent, but it is possible that there is an unusual overrepresentation of A1AR in afferent arterioles of the very superficial nephron population. Concordant with a tonic constrictor effect of adenosine in these nephrons are observations showing that inhibition of A1AR with 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) or CVT-124 caused afferent arteriolar vasodilatation and an increase in both SNGFR and kidney GFR (5, 41, 86).
The effect of adenosine on arteriolar tone has been studied more directly in preparations that permit visualization of vessel diameters and that are not restricted to a selected population of vessels. Furthermore, in these in vitro preparations, the testable adenosine concentrations include the subnormal range, thereby facilitating the detection of A1AR-mediated effects. In afferent arterioles of neonatal hamster kidneys transplanted in the cheek pouch of adult animals, adenosine, topically applied through micropipettes, caused dose-dependent vasoconstriction of afferent arterioles, whereas it dilated the arterioles of the cheek pouch itself (30). In isolated perfused afferent arterioles from the rabbit, addition of adenosine to the bath caused vasoconstriction in a dose-dependent fashion (84). Effects consisted of a 30% reduction in vessel diameter in proximal parts of the arteriole with maximum effects being reached at 10–6 M and smaller effects at higher concentrations, indicating that in this part of the arteriole A1AR-mediated vasoconstriction is partially counteracted by A2bAR-dependent vasodilatation as adenosine concentrations increase. It is consistent with this interpretation that the vasoconstriction caused by the A1AR agonist CHA was slightly greater than that caused by adenosine and that it increased over the entire concentration range from 10–9 to 10–4 M (84). However, in the afferent arteriole in the immediate vicinity of the glomerulus, adenosine caused a monotonic vasoconstriction consisting of a 45% reduction in vessel diameter at 10–4 M, the highest concentration tested (Fig. 1). The absence of a discernible vasodilator effect at concentrations at which A2bAR should be activated indicates that the short section of the afferent arteriole close to and inside the glomerulus is unique in that A1AR-induced constriction does not appear to be opposed by A2AR to a detectable extent. Recent experiments in isolated afferent arterioles from the mouse indicate a similar effectiveness of abluminal adenosine to vasoconstrict the vessel, particularly at its glomerular entrance segment. The origin of the arterioles used in both the rabbit and mouse studies was the midcortical and outer cortical region, so that arterioles from true juxtamedullary nephrons were not included. Our results are apparently different from the net vasodilator effect of CHA in the isolated perfused kidney that was seen at perfusate concentrations of 10–5 M and higher (43, 46). Thus the A2AR activated by high CHA concentrations and determining total renal vascular resistance in the whole kidney are localized on vascular segments other than afferent arterioles.
In the hydronephrotic kidney preparation, another technique permitting direct observation of arteriolar responses, the effect of adenosine appears to be transient. With topical application, adenosine caused a dose-dependent vasoconstriction over the 10–6 to 10–4 M dose range that faded within 1–2 min, and a similar effect was seen in an in vitro perfused hydronephrotic kidney with luminal application (20, 78). There was no noticeable steady-state effect of adenosine in the afferent arterioles, whereas interlobular arteries and efferent arterioles showed steady-state vasodilatation at a concentration of 10–5 M (20). The abluminal administration of CHA, in contrast, had effects comparable to those found in isolated vessels. These effects consisted of a stable diameter reduction that was dose dependent in the range between 10–8 and 10–6 M and that was most pronounced in the distal part of the arteriole where it caused a maximum effect of about –50%. The reduction in vascular diameter was accompanied by a reduction in glomerular blood flow by 30–40% at 10–7 M and by >50% at 10–5 M (15, 27). Although NECA vasodilated all preglomerular vascular segments up to the arcuate arteries, it caused no change or even a small constriction in the distal afferent arteriole (16, 27). Although NECA is not a specific A2 agonist, this finding provides additional support for the notion that the distal afferent arteriole is unique in its predominant expression of A1AR. In view of the normal actions of CHA, the waning effect of adenosine in this preparation may reflect an increased expression of dilatory A2AR. It is also of note that at least in the in situ hydronephrotic kidney model the starting level for the adenosine addition studies are the prevailing tissue and plasma adenosine levels, not an adenosine-free condition.
Juxtamedullary afferent arterioles. Studies of the effect of adenosine in juxtamedullary arterioles are important in view of the notion that medullary blood flow may be regulated by adenosine in a way that is opposite to cortical blood flow regulation. Juxtamedullary afferent arterioles, studied in a blood-perfused preparation, respond to abluminal application of adenosine at 10–6 and 10–5 M with a marked transient and a smaller steady-state reduction of vessel diameter that was prevented by the A1AR antagonist KW-3902 and magnified by A2aAR inhibition (11, 28, 47). At concentrations >10–5 M, the effect of adenosine was vasodilatation of juxtamedullary afferent arterioles that was partially inhibited by the A2aAR antagonist KF-19837 (47). Diameter evaluations in these studies were made at a distance of 100 μm from the glomerulus and did not distinguish between proximal and distal regions of afferent arterioles. Although the steady-state effect of adenosine in these studies was relatively small, it may be relevant to point out that a 10% reduction in vessel diameter translates into a 50% increase in vessel resistance.
The response of afferent arterioles of juxtamedullary nephrons to CHA in the hydronephrotic kidney preparation consisted of a dose-dependent diameter reduction in the tested concentration range of 10–8 to 10–6 M that was about one-half that seen in more superficial arterioles (16). Concomitantly, glomerular blood flow was reduced by ∼40% at 10–6 M, a response that was smaller than seen in superficial nephrons. In contrast to superficial arterioles, NECA had a small dilator effect in juxtamedullary afferent arterioles. These studies indicate that afferent arterioles of juxtamedullary nephrons may be less responsive to adenosine than arterioles from superficial or midcortical nephrons but that they respond qualitatively similar. Based on the functional information furnished by CHA and NECA, one would conclude that afferent arterioles of juxtamedullary nephrons have a lower expression level of functional A1AR and a higher level of A2AR compared with superficial arterioles (16). Nevertheless, the dilator action of A1AR inhibition indicates that, in juxtamedullary afferent arterioles, the dominant effect of adenosine up to a concentration of 10 μM is vasoconstriction.
It is unclear to what extent a loss of A1AR-mediated constrictor efficiency is responsible for the fleeting reduction in total renal blood flow caused by systemic adenosine, but the following aspects seem pertinent. The maintenance of constriction in afferent arterioles for extended periods of time noted in the observational studies indicates that A1AR in afferent arterioles do not undergo rapid desensitization, the waning of a functional response during prolonged or repeated exposure of a receptor to its ligand (27, 30, 47). Most notably, in recent experiments in isolated afferent arterioles from the mouse, vasoconstriction caused by adenosine was observed to last for up to 30 min (Hansen PB, unpublished observations). The persistent nature of the A1AR-induced vasoconstriction of afferent arterioles is consonant with the evidence from a number of studies indicating that the desensitization of native A1AR in response to prolonged exposure to an agonist occurs in a time frame of hours to days (60). Furthermore, the inhibition of forskolin-stimulated adenylate cyclase activity in CHO cells expressing the human recombinant A1AR was unaffected by a 30-min treatment with an A1AR agonist (59). We consider it unlikely that the propensity of A1AR to desensitize varies between different preparations and between A1AR expressed in different segments of the renal vasculature.
Because the adenosine effects in vivo are assessed in a more complex environment than those encountered in vitro, it is possible that differences in the presence of some modulating factor account for the apparent difference in the constrictor potential of adenosine seen in vivo and in vitro. The most intensely studied modulator of A1AR-mediated constrictor actions is ANG II. There is abundant evidence to show that a reduction in ambient ANG II levels and the prevention of ANG II formation and action cause a marked attenuation of the vasoconstrictor response of the intact kidney to adenosine (15, 23, 56, 73, 85). Conversely, an elevation of ambient ANG II concentrations enhances the constrictor effect of A1AR activation by adenosine or A1AR-specific ligands (56, 85). Nevertheless, it is not clear that differences in ambient ANG II levels can explain the different responses of intact kidneys and isolated preparations. One would expect ambient ANG II concentrations to be lower in the artificial environment, and adenosine responses should therefore be blunted, the opposite of what is actually observed. The possibility that A1AR-mediated vasoconstriction is dependent on the state of arteriolar innervation is not supported by studies showing an unaltered constrictor response to an A1AR agonist in denervated compared with innervated kidneys (61). These results do not lend support to the possibility that the absence of nervous input in the isolated preparations importantly modifies their adenosine response.
Because the studies examining the effect of adenosine on renal blood flow in the whole kidney have been performed during systemic administration of adenosine, whereas the in vitro experiments were typically done during abluminal adenosine application, the possibility exists that the strength of the constrictor response varies with the route of administration. In support of a sidedness in the vascular actions of adenosine, we recently observed using laser-Doppler flowmetry in mice that adenosine given intravenously caused an increase in superficial renal blood flow, whereas the infusion of adenosine in the interstitial region below the flow probe caused a reduction in blood flow (Hashimoto S, unpublished observations). Furthermore, the vasoconstriction of isolated perfused afferent arterioles from the mouse caused by the bath addition of adenosine was not seen when adenosine was added to the luminal perfusate (Hansen PB, unpublished observations). In a study comparing the effects of intravenous infusion of high- and low-molecular-weight polyadenylic acids on renal blood flow in dogs, it has been noted that the low-molecular-weight compound (mol wt 5,000) caused transient vasoconstriction like adenosine, whereas the high-molecular-weight compound (mol wt 100,000) caused an exclusive and long-lasting vasodilator response that was inhibited by theophylline (79). The authors concluded that adenosine causes A2AR-mediated vasodilatation through an intravascular site, whereas the A1AR causing vasoconstriction are normally accessed from the interstitial aspect of the vessel. The causes for this sidedness of the effect of adenosine need to be explored further. It is conceivable, although unproven, that A1AR are present in endothelial cells along the renal vasculature and that adenosine causes the release of nitric oxide (NO) and perhaps other endothelial vasodilators when administered from the vascular but not from the interstitial aspect of the vessel. The resulting A1AR-induced constriction would therefore be blunted by endothelial factors only when adenosine is given intravascularly. In a study in dogs, the administration of nitric oxide synthesis (NOS) inhibitors caused a marked augmentation in the constrictor response of renal blood flow to bolus injections of adenosine while the dilator effect of the A2 agonist CGS-21680 was unaffected, indicating that adenosine may cause NOS activation through an A1AR-mediated mechanism (52). Enhancement of A1AR agonist induced vasoconstriction by NG-nitro-l-arginine methyl ester, and a marked left shift of the dose-response relationship between adenosine concentration and vasoconstrictor response has also been observed in the rat (7, 63). Studies showing a similar left shift in the adenosine dose-response curve during application of indomethacin suggest that a vasodilator prostaglandin may be another endothelial factor opposing A1AR-mediated constriction (62). The results of these studies do not establish that A1AR activation is directly coupled to the release of NO or prostaglandins since they are also compatible with the possibility that the constrictor effect of adenosine is merely enhanced by the removal of a constitutive vasodilator influence. It is also of note that adenosine administered in the vascular space must cross the endothelial cell layer to interact with smooth muscle cells. In addition to being a potential physical barrier to the movement of adenosine, endothelial cells from coronary blood vessels have been shown to rapidly metabolize adenosine with incorporation into various nucleotide pools (45). These authors suggest that, in coronary vessels, transvascular adenosine movement may be impeded more by this metabolic barrier function of the endothelium than by its physical properties. If the endothelium restricts the movement of adenosine, one would expect differences in receptor accessibility dependent on the route of administration.
In summary, adenosine administered from the vessel outside causes a marked, nontransient vasoconstriction in afferent arterioles from all regions of the kidney, although vessels of superficial nephrons appear to be more sensitive than arterioles of juxtamedullary nephrons. In the afferent arteriole at the glomerular entrance, the diameter reduction is monotonically dose dependent, indicating the absence of adenosine receptors opposing vasoconstriction. In the more proximal part of the arteriole, the vasoconstrictor effect of adenosine is blunted (at lower concentrations by A2aAR and at higher concentrations by A2bAR), but net vasodilatation does not occur. In the hydronephrotic kidney preparation, the adenosine-induced vasoconstriction is transient, an effect that may reflect changes in the vascular response pattern resulting from chronic elimination of the tubular epithelium. For reasons that are not entirely clear, A1AR activation appears to cause a more pronounced constriction of afferent arterioles when added to the interstitial aspect of the vessel.
Effect of Adenosine at the Organ Level
In contrast to bolus injections, adenosine administered by constant infusion is associated with an unchanged or usually even increased renal blood flow (23, 54, 58, 77). The causes for the steady-state vasodilatation have been ascribed to preferential relaxation of the efferent arteriolar or medullary vascular beds, but a convincing argument for either explanation cannot be made on the basis of studies at the organ level. Nevertheless, the selective A2AR agonist CGS-21680A elicits a monophasic reduction in renal vascular resistance, clearly indicating that activation of A2AR is the cause for the transient nature of the renal constrictor response to adenosine (35). Furthermore, vasodilatation was seen in isolated perfused kidneys with the somewhat A2AR-specific agonist NECA (43, 46). It is noteworthy that GFR is typically suppressed by adenosine in a more persistent fashion so that a reduction of filtration fraction is an invariable consequence of prolonged adenosine administration.
Even though obvious, it is relevant to point out that the infusion studies discussed above examine the effect of an addition of adenosine to the existing endogenous nucleoside levels and therefore limit the analysis to the supranormal concentration range. A consideration of the baseline adenosine concentrations in plasma and in the renal interstitial fluid may therefore be helpful to predict the expected changes in receptor engagement with adenosine infusions, taking into account the known affinity and dissociation constants of the different adenosine receptors. Plasma adenosine levels have been reported to be somewhere between 100 nM and 1 μM, i.e., in the 10–7 to 10–6 M range (12, 18, 32, 89, 91). Renal interstitial concentrations of adenosine as determined by microdialysis have been found to be between 50 and 200 nM in the cortex and between 160 and 210 nM in the medulla (6, 48–50, 70, 92). Thus these levels are in the same order of magnitude as plasma concentrations. The classical early analysis of ligand binding kinetics to the various adenosine receptors has established that A1AR and A2aAR have affinity constants for adenosine in the order of 10–8 M, whereas the affinity of A2bAR is much lower, around 10–5 M (14, 19, 37, 82). Thus, at the prevailing extracellular adenosine concentrations of ∼10–7 M, one would expect A1AR and the high-affinity A2aAR to be partly occupied, whereas A2bAR are probably not. The absence of a major effect of nonspecific AR inhibitors such as theophylline or aminophylline on renal hemodynamics is consistent with the notion that resting renal vascular tone represents a state of balanced A1AR and A2aAR activation (9, 54, 64). The increments in adenosine concentration resulting from the infusion should mostly be targeted to the A2bAR receptor pool. For this simple reason, it is perhaps not surprising that adenosine infusions result in relaxation of all vessels expressing A2bAR, the majority of the renal vasculature, and therefore cause global renal vasodilatation. In view of the evidence discussed above that the afferent arteriole near the glomerulus may not vasodilate even at elevated levels of adenosine, at least when adenosine is administered from the interstitial side, it is relevant to point out that the afferent arteriole is not the only resistance vessel in the kidney. Aside from the significant contribution of the efferent arterioles, interlobular arteries in the rat kidney have been estimated to represent as much as 50% of renal preglomerular resistance (8, 26) and have also been shown to contribute importantly to autoregulatory adjustments of renal vascular resistance (25). Furthermore, the renal artery has been shown to regulate renal vascular resistance by the release and downstream action of endothelium-derived vasodilators (31). Therefore, global renal vasodilatation may well occur in the absence of overt vasodilatation in afferent arterioles.
It is now well recognized that the majority of vasodilator agents act by binding to their receptors on endothelial cells and by eliciting the generation and release of endothelial relaxing factors, most notably NO, endothelial hyperpolarizing factor, and prostaglandins. The presence of A2AR in endothelial cells of the renal vasculature has not been established directly, but a number of studies in various excised vessel preparations indicate that adenosine-induced vasodilatation is probably to some extent endothelium dependent. In the majority of these studies, adenosine appears to augment NOS activity and NO release through an A2AR-mediated process, an action that would enhance the dilator component rather than diminish the constrictor component of the adenosine actions (1, 21, 38, 75, 90). In addition, adenosine has also been reported to dilate rabbit renal arteries through an endothelial relaxing factor that does not appear to be NO (66). Finally, adenosine has been shown to consistently stimulate the production of NO in cultured endothelial cells, usually through an A2AR-dependent mechanism (36, 53, 87). Thus, in addition to the possible blunting of A1AR-induced vasoconstriction as discussed above, endothelial dilator factors generated in response to A2AR activation may enhance renal vasodilatation, thereby contributing to the waning renal constriction in the kidney during intravenous administration.
The overall conclusion from these studies at the organ level would be that the intravenous administration of exogenous adenosine, i.e., an elevation of plasma adenosine concentrations above normal, causes a short-lasting net vasoconstriction mediated by high-affinity A1AR. However, this effect is overcome, at the elevated plasma adenosine levels resulting from the addition of exogenous nucleoside, by the simultaneous activation of lower-affinity A2AR so that the dominating and lasting effect is net vasodilatation in most cases.
Effect of Adenosine in Efferent Arterioles
Dilatation of efferent arterioles has been suggested as one of the reasons for the return of renal blood flow to normal or supranormal values during an adenosine infusion, a notion that is mainly based on the observed reduction in filtration fraction (42, 77). However, it has been difficult to establish an unequivocal vasodilator action of adenosine in preparations in which the arteriole can be observed directly. In the blood-perfused juxtamedullary nephron preparation, the effect of adenosine on the diameter of efferent arterioles was qualitatively similar to that seen in afferent arterioles consisting of a stable diameter reduction by ∼6% at a concentration of 10–5 M, a constrictor effect that was smaller than that seen in afferent arterioles (11, 47). Vasodilatation in the presence of an A1AR blocker, and enhanced constriction in the presence of an A2aAR blocker, resembled the effects noted in afferent arterioles. On the other hand, in the hydronephrotic kidney, adenosine at 10–5 M caused a steady-state diameter increase of ∼14% that was not changed much by the A1AR antagonist DPCPX but was abolished by the A2AR antagonist 3,7-dimethyl-l-propargylxanthine (20). These results suggest the absence of A1AR in efferent arterioles in this preparation, a notion supported by previous reports using the same preparation in which the A1AR agonist CHA caused only small or no diameter reductions in efferent arterioles up to a concentration of 10–5 M (16, 27). In contrast, NECA induced a small efferent vasodilatation and an increase in glomerular blood flow (27). Thus adenosine effects in the efferent arteriole are not very pronounced and appear to consist of small constrictions at lower and small dilations at higher concentrations. The small magnitude of both constrictor and dilator effects suggests rather low levels of expression for all receptor subtypes. Overall, we conclude that a dilator effect of efferent arterioles may contribute to the loss of net vasoconstriction at elevated adenosine levels but that it is unlikely to account for the full dilator action of adenosine.
Adenosine and medullary blood flow. Vasodilatation of the vessels controlling renal medullary blood flow has been proposed as being responsible for the net vasodilatation of the kidney in response to continuous intravenous infusion of adenosine. Renal blood flow distribution measured with microspheres showed an increase in inner cortical blood flow, whereas outer cortical blood flow was unchanged (72). The magnitude of this increase varied between 23 and 94%, depending on the renin status of the dogs. Interstitial infusion of adenosine induced an increase in medullary blood flow measured with laser-Doppler flowmetry by ∼40% (2). Direct infusion of adenosine in the renal medulla caused an ∼25–30% increase in both outer and inner medullary blood flows (92). Direct assessment of blood flow in single inner medullary vasa recta by videomicroscopy showed an increase in red cell velocity without a diameter change only during intrarenal adenosine infusion at the highest dose tested (39). The infused amounts did not induce significant changes in inulin or p-aminohippuric acid clearances. In isolated perfused outer medullary vasa recta, the administration of increasing concentrations of adenosine induced a biphasic response, consisting of a vasoconstriction in the dose range between 10–11 and 10–7 M and a vasodilatation at 10–6 to 10–5 M (68). In contrast to cortical resistance vessels, administration of adenosine to vasa recta preconstricted by ANG II leads to vasodilatation (68, 69). The concentration of adenosine in the interstitial fluid of the medulla is between 10–7 and 10–6 M, a level where one may expect not much impact on resting tone but where an increase of adenosine concentration should cause vasodilatation (70, 92). In summary, most studies agree that the administration of adenosine causes an increase in medullary blood flow by relaxing both juxtamedullary afferent and perhaps efferent arterioles and outer medullary vasa recta pericytes. Nevertheless, for quantitative reasons, we consider it unlikely that this increase in medullary blood flow can be the only reason responsible for the overall increase in total renal blood flow seen with constant infusions of adenosine. Medullary blood flow represents only ∼10% of total renal blood flow. Thus a reduction in cortical blood flow by 50% would require a more than fivefold increase in medullary flow for compensation. The magnitude of the observed increase in medullary blood flow, variable as it may be, is not even close to this expectation. Thus much of the compensatory increase in total renal blood flow in response to continuous adenosine infusions must take place in the renal cortex.
In conclusion, the intravenous infusion of adenosine, i.e., an increase of plasma adenosine levels above normal, causes a renal vasodilator response that is the result of A2AR-mediated vasorelaxation in most parts of the renal vasculature, including larger renal arteries, juxtamedullary afferent arterioles, efferent arterioles, and medullary vessels (Fig. 2). A combination of these effects, rather than one single action, is responsible for the relaxation caused by exogenous adenosine in the whole kidney. A2AR-mediated vasorelaxation may be facilitated by intravascular receptors, most likely on endothelial cells, causing the release of NO and other endothelial relaxing factors. In contrast, the afferent arteriole, especially in the segment closest to the glomerulus, responds to adenosine with vasoconstriction over a wide concentration range. Afferent arteriolar A1AR are selectively activated from the interstitial aspect of the vessel, a characteristic that is ideally suited for the presumed physiological role of these receptors, the mediation of the TGF response.
Work from the authors' laboratory was supported by intramural funds from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). P. B. Hansen was the recipient of a Visiting Fellowship of the NIDDK.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
- Copyright © 2003 the American Physiological Society


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A woman had a necklace snatched from her neck while walking along The Slipe on with her baby in a pram.
The incident happened on Tuesday, July 22 at about 2.15pm between the double bridges over the footpath and the new footbridge that goes over to the Bedford Road, as she walked towards Bedford
from Queen's Park.
The woman could hear a bicycle coming up behind her and stepped to one side to let it
However the rider then snatched the necklace – made of Russian gold – from her neck – nearly spinning her and the pram into the water as he did so.
The necklace broke and the man carried it off with him on the bike.
Investigating officer Gary Maxey would like to hear from anyone who saw this or was down on the footpath at the time.
He can be reached through the 24 hour police non-emergency number 101, or text the force control room direct on 07786 200011. Alternatively, call independent charity Crimestoppers on 0800 555111. You do not have to give your name and no-one will know you called.


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Why Facebook's $19b Purchase of WhatsApp Makes Sense
Kids have been snubbing this online version of a dinner table. But this deal is a door back to the kids, and to a billion more users.
The announcement that Facebook is buying mobile-messaging startup WhatsApp for $19...
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Things that are popular all over the world and become a rage take quite some time to come to India. The international trends and excitement always have a delayed reaction in our country. In some cases you don't even realize what options you have while planning a holiday. Adventure freaks plan their holidays abroad around various activities they get to do. Little do they know, they don't actually have to trek half way across the world. More and more options for recreation, holiday and sport are available so you can plan your travel within the country and enjoy yourself.
Zorbing - Remember those dreams where you often find yourself free falling. Now, you can literally chase that dream with a thrilling new sport knows as Zorbing. Widely popular all over the world, it has has now found a home in India as well. Of course safety precautions are taken and you're heavily strapped inside the ball to avoid any injury. So, if you're looking for some major adrenaline rush, you will surely enjoy this ball of thrill.
Image Credit: www.theworldatyourfeet.wordpress.com
Kite Surfing – A combination of water sport, gymnastics, surfing , paragliding and many other, the idea of being harnessed to a power kite is a high on its own. The movement of the kite is completely dependent on the velocity of the wind and yes, it sounds as risky as it looks. It might be a little difficult but not impossible to indulge in some kite surfing in India; a country where this sport still has a lot of catching up to do. It's also one of the fastest growing water sports in the world. So if you like the thrill of high tide and water, then this one is right up your alley.
Image Credit: www.theboardroomadventures.wordpress.com
White water rafting – Powering and canoeing your way through an intense gushing river is what White water rafting is all about. It's an intense recreational sport that gets you pumped up so high the minute you're out of the raft that it makes you feel all mighty invincible. An adventure sport which could be performed in a group or solely, trick is to make sure you don't topple over while rowing as that can get exceedingly dangerous. Then again, if there isn't any element of danger at all, where's the fun in that!
Image Credit: http://i208.photobucket.com/
Bungee Jumping - The thrill of jumping off a ledge, harnessed by your legs, and dangled upside down is a feeling that is hard to explain. The rush is easily addictive and one of the reasons that makes people go at it again and again. A great way to also overcome the fear of heights, if you are itching for something fun, this is the perfect sport for you. Also you don't have to fly to another country to jump in the air, just find your way to Lonavala.
Image Credit: www.hdwallpapersci.com
Scuba Diving - A certain amount of training is required before diving your way in to the under world . It's a recreational experience one needs to go through at least once. The view is undeniably breathtaking and a sense of calm and serenity spreads inside you. You don't need to fly off to Malaysia or South Africa for this experience now as India too has been christened a home for several new dive spots. You just have to find them!
Image Credit: students.stedwards.edu
Zorbing and Bungee jumping can both be found at Della Adventure Sports in Lonavla near Mumbai. Kite Surfing can be found in Goa. White Water Rafting is extremely popular in Rishikesh and Deep sea diving is available all over Andaman islands as well as Lakshadweep.
So what's holding you back. You don't need a passport or a visa, just some company and a little spontaneity.
Article by - Roxanne Bamboat


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Chris Geith (pronounced "guy-t") is one of the lucky few who actually knew what he wanted to do with the rest of his life from the moment he was able to climb up on a piano stool and sit beside his father. He would watch his father move his nimble fingers across the black and white keys of the piano with agility and total awareness of where those fingers needed to be to make beautiful sounds. Knowing how to make beautiful sounds with the piano gave meaning to life in young Geith's eyes.
"My father was always playing the piano and the organ when I was a little kid, and I wanted to be able to play like him. He would let me experiment on his piano, and by the time I turned 8, he gave it to me, so I could start studying music. He would later take me to all kinds of jazz clubs in Italy where I would see great musicians and get even more inspired."
Though Geith's father passed away seven years ago, Chris never imagined of burying the talent that his father nurtured in him. It would be the impetus which gave Chris something to say as a solo artist. "For many years I've backed up all kinds of singers and horn players and it's all been great experiences, but when you realize you have something to say yourself, it's time to move to the front of the stage."
Prior to becoming a solo artist, Chris Geith was a star pupil in school and excelled in music classes. "I went through a lot of music training over the years, first, the Conservatory of Music in Milan, and later, The Manhattan School of Music, but I'm self-taught on some things like, in example, orchestration and arranging. The most helpful thing in the beginning for me was to listen to a lot of music and analyze all the different parts."
His education exposed him to everything from classical to modern piano and from jazz to experimental music, but learning good technique was imperative. "If you've learned the right technique playing the piano, you can play to 8 hours without ever getting stiff or tired. The best playing always comes from staying relaxed."
He cites a turning point in his life when, "My father gave me the opportunity to study at The Manhattan School of Music, so I got my masters degree there. It was a great experience. I was coming up with some unusual arrangements for popular standard tunes. Some of the teachers loved what I was doing and some, I guess, kind of didn't - the more conservative ones," he mutters, "but in the end, I graduated one semester earlier with 'advanced standing.' I went into contemporary jazz because there are a lot more possibilities, musically speaking. The pop/rock [style]," he purports, "this can be fun but there is only so much you can do harmonically."
He reveals, "I've been playing jazz since I was 14. My father was a jazz fanatic and really got me into it. There really hasn't been a specific 'big break,'" in Geith's opinion, "it's just been an ongoing journey."
He recalls, "My early musical experiences were playing with a lot of different bands in all kinds of clubs and collaborating with many music production companies'recording studios in New York City and in Milan, Italy." Some artists whom he backed up include Julie Andrews and Paul Anka.
His first taste as a solo artist happened in 1995 when Keyboard Magazine awarded him the top spot for his composition "Sunrise Hunter" at their 20th Anniversary Keyboard Competition. He describes, "Like all the rest of my tunes, the writing was a very spontaneous process, I just felt like writing something up tempo with a cool groove and horns. The title was just a coincidence, it just felt right for the track."
The single would be on his debut album, Forever Again released by the European label Arta Records. He shares, "Forever Again was a collaboration with trumpet player Laco Deczi. He's a famous musician over in Europe and hooked us up with Arta Records in Prague. The music would probably have been in tune in the USA also, but the labels we had shopped it to, had turned it down."
He attests about Arta, "Our label never asked anything from us. It was nice to have some distribution over there, but the marketing has been fairly limited."
Geith provides, "I produced the album over a long period of time - about two years. As I mentioned, it was a collaboration with trumpet player, Laco Deczi and his son drummer, Vaico Deczi. I'm very proud of this album, there is a tremendous amount of chemistry going on in the music. It's a very 'orchestral' project, but with a lot of interesting grooves going on at the same time." He synapses, "Very upbeat but also mellow."
In 2001, Geith released his second solo album, Prime Time under the moniker The Chris Geith Group. He explains, "It's always an experimentation to some degree. To me music is all about the 'feel.' I write what I feel. Melody is very important to me, but so are interesting chord progressions. When I write music, and I find myself with a smile on the face, I know I've got something going. I like to create moods and have variety from song to song. There will be upbeat, happy sounding tunes and then there will be some other songs that might make people cry, and if they do, I know I've touched somebody's heart."
He examines, "Making albums is a very complex thing for me. I question every note and every sound a million times, but when the process is completed, I generally have something good in my hands, or at least I hope so!"
For his latest album, Timeless World, he reflects how he really wanted to make a piano-central album with a modern flare as he handled all piano, keyboard, and program parts. "Timeless World took over two years to complete. I wanted to make a piano album with a lot of orchestration around it. I like the combination of acoustic piano and lush string sounds and then put a cool groove underneath it. The tune 'So Many Nights' is a good example of that. In the 'tradition' of the previous album, I wanted to have an extensive variety of moods."
He discusses how the music pollinates during the songwriting process, "Timeless World includes tunes I've written over several years. I tend to work on my music just like a full time job. I don't just wait for inspiration to fall from the sky, although sometimes it does," he beams. "I'll try different things for hours until I start to feel some chemistry. I will come up with a ton of ideas and use only a small percentage of it."
The musicians who played on Timeless World were friends of his. He expresses, "My friend, guitarist Matt Marshak, founder of Nuance Music Group, did some awesome guitar work, and my friend Fred Scerbo did all the saxophone tracks which all added a lot to the project."
Other musicians who played on Timeless World include Mark Mullers (bass), Donny D (drums, percussion), Dean Kosh (drums on Restless Heart), and Al Davis (trumpet, trombone). Geith tells, "I like playing with good musicians and make the music sound tight and fun, it does motivate me to write. Matt Marshak, Fred Scerbo and Dean Kosh are for sure musicians I enjoy playing with. Of course, there are a lot more people I enjoy working with, but it's hard to make a list with so many great musicians."
One noticeable aspect about Geith's arrangements is that while he is composing them, he thinks about how they would sound performed live in front of an audience. "I always imagine 'playing live' when I write. I like to picture the reaction of the audience when the music becomes more and more intense." When asked whether the songs on Timeless World were inspired from playing live, he admits, "Yes, it has. I would say most of it."
Now that Timeless World is out, Geith says that plans for a tour are underway. "There are plans in the works for touring. In my case, taking the music on the road is a complex operation as it requires a lot of technical support." He reminisces, "Some of the most incredible moments have been playing in Italy underneath old castles and in big parks in front of huge audiences."
Since Geith not only handles the piano and keyboard parts, but also the program arrangements on the recordings and live on stage, I had to ask if he ever worries about programs taking the place of his piano playing. He responded, "That will never happen. No technology will ever be able to 'replace' Chris Geith," he smiles.
Some aspects about Chris Geith's contemporary jazz album Timeless World are old-fashioned, just like his father would have done it, and others are quite innovating and able to keep up with a modern age. The melodies are tuneful and atmospheric as they represent the moods of the world. It seems that making music for people to carry in their bosoms is Chris Geith's forte.


text: You are here: Home > Course > Accompaniments > Chutney > Tomato Chutney ( Cooking with 1 Tsp Oil) Tomato Chutney ( Cooking with 1 Tsp Oil)by Tarla Dalal 26 Nov 2012 You are not signed in. Please sign in to access your cookbooksExisting members click here to sign inNew visitors click here to sign up Please sign in to create shopping lists! 4/5 stars 100% LIKED IT 4 REVIEWS ALL GOOD Added to 398 cookbooks This recipe has been viewed 99813 times This tangy chutney is the best combination for bland dishes like Idli and appe! One of the most popular South Indian chutneys, this is sure to perk up any meal it is served with. Purée the mixture of sautéed tomatoes, onions and dals a bit coarsely, to enjoy a chunky salsa-like texture. The best part is that this delectable Tomato Chutney is made with just a single teaspoon of oil and no other fatty ingredients, so it is a real guilt-free treat! Add your private note Tomato Chutney ( Cooking with 1 Tsp Oil) recipe - How to make Tomato Chutney ( Cooking with 1 Tsp Oil) Tags ChutneyLow Cal Pickles/ Sauces / ChutneysMixerChutneysVitamin B9 Rich FolateLow Calorie Chutneys Preparation Time: 5 mins   Cooking Time: 9 mins   Total Time: 14 mins     Makes 0.50 servings Show me for servings Ingredients 1 cup chopped tomatoes1 tsp oil1/2 tsp chana dal (split bengal gram)1/2 tsp urad dal (split black lentils)8 to 10 curry leaves (kadi patta)1 tsp finely chopped green chillies1/4 cup chopped onions1/4 tsp turmeric powder (haldi) salt to taste Method Heat the oil in a broad non-stick pan, add the green chillies, chana dal, urad dal and curry leaves and sauté on a medium flame for a few seconds.Add the onions and sauté on a medium flame for 2 to 3 minutes.Add the tomatoes, turmeric powder and salt, mix well and cook on a medium flame for 4 to 5 minutes, while stirring occasionally. Keep aside to cool completely.Once cooled, blend it in a mixer to a coarse mixture.Serve or store refrigerated and use within 2 days. Other Related Recipes Accompaniments Buckwheat Dhokla, Faraal Buckwheat Dhokla Mag Na Dhokla Sooji Idli / Suji Idli Veg Stufffed Idlis Nutrient values per tablespoonEnergy 16 kcalProtein 0.4 gmCarbohydrate 1.8 gmFat 0.8 gmFibre 0.5 gmFolic Acid 8.0 mcg RECIPE SOURCE : Cooking with 1 Teaspoon of Oil


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Cuba marks Easter as public holiday
03:32pm | Fri, April 06, 2012
Communist Cuba is marking Easter with a public holiday Friday, for the first time in decades. This follows Pope Benedict's visit to the country last week, where he requested the move.
Religious holidays in Cuba were cancelled after the 1959 revolution, and fewer than 10-percent of Cubans are practising Catholics.
Nonetheless, the Church is the most influential organization outside the Communist government.
The Cuban government said it granted the request as a mark of respect, and to commemorate the "transcendental nature" of the Pope's visit. The Pope's predecessor, John Paul II, made a similar request during the last papal visit to Cuba in 1998, successfully persuading then-leader Fidel Castro to recognize Christmas as a public holiday.


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MC 1-226, PO Box 20345Houston, TX 77225-0345832-355-2666; FAX 832-355-6500E-mail: firstname.lastname@example.com
Hospital affiliations: CHI St. Luke's Health-Baylor St. Luke's Medical Center
Academic appointment: Clinical Assistant Professor, Baylor College of Medicine.
Medical school: University of Osteopathic Medicine, 1991, Des Moines, Iowa.
Specialty training: Cardiothoracic Anesthesiology Fellowship, Cleveland Clinic Foundation, Cleveland, Ohio.
Certification: American Board of Anesthesiology.
Specialty interests: Cardiovascular anesthesiology.


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The Movie:
Atom Egoyan("The Sweet Hereafter")'s 1994 film did not recieve the same attention that "Hereafter" did, but it has gained a cult following from fans of the director. It's unfortunate that Miramax sold the film as if it was some sort of late night cable thriller, because it's far more than that. "Exotica" spins around a nightclub where a group of characters are brought together through ties to the club. We're introduced to the characters; Christina, a young dancer who performs often for a lonely auditor named Francis (Bruce Greenwood); Thomas, a pet-store owner and the DJ of the club; played very well by Elias Koteas, who was also excellent in "The Thin Red Line". Through jealousy and emotion, the story falls back on itself, making these people who seemed like strangers closer and closer together. As details are revealed, layers come into view. These are not bad people, these are lonely people who are in pain. Francis and Christina share an unspoken bond, and he wants nothing more than to have her in front of him. While these characters intentions seem at once simple, there is always the feeling as if there's more that's still unsaid. It's that unsure feeling of what will happen next that makes "Exotica" watchable.
By the end, everyone may not be sympathetic for these characters, but the story has pulled the threads of their tales together in an interesting and entertaining way with a suprising ending. Good performances, fine writing and excellent direction make "Exotica" worth a rental if you're a fan of Egoyan's work and never saw this film, or if you're a fan of darker character films like this. "Exotica" also features an early performance from Sarah Polley, who was fantastic in this year's "Go".
The DVD
VIDEO: Not unwatchable, but not terribly pleasing either. Watching a lot of it makes you wish that this film had been distributed by New Line, who distributed Egoyan's "Sweet Hereafter" and did a far more impressive job with it. Images are soft and although some scenes fare better than others, it's still rather dissapointing. Colors are not terribly rich and remain subtle throughout, but have no major problems. Detail is ok, although it definitely is lacking in some of the dimly lit scenes.
Although there is no shimmering, some of the film has a slightly grainy appearance and there are a few noticable marks in the print used. All in all, picture quality that's consistently mediocre and definitely soft throughout. Not the worst I've seen from Disney, but definitely not as good as this film could look. The box says that the film is presented as 1.66:1, but the film is definitely 1.85:1 on this DVD.
SOUND: The cool, creepy score by Mychael Danna (who also did the score for "8mm") sounds rich and strong, but that's pretty much the biggest element of the audio. Dialogue is fine, although occasionally it isn't as easily understood as I would like it to be.
MENUS:: Basic menu art based on the cover art.
EXTRAS:: None - the norm for Disney catalog titles.
Final Thoughts:May be worth checking out as a rental - hopefully will make a comeback as a "Miramax Special Edition", although it's probably doubtful.