88695
document
Differential effects of angiotensin converting enzyme inhibitors on the vasodepressor and prostacyclin responses to bradykinin . Angiotensin converting enzyme ( ACE ) inhibitors block degradation of bradykinin and bradykinin stimulates prostacyclin production . ACE inhibitors are reported to increase prostaglandins . Therefore , we set out to determine 1 ) the contribution of prostacyclin to the bradykinin-mediated vasodepressor effects of ACE inhibitors , 2 ) whether ACE inhibitors alter the effect of bradykinin on prostacyclin , and 3 ) whether the effects of ACE inhibitors on bradykinin and prostaglandins are class effects or dependent on ACE inhibitor structure . To address these questions , we compared the effects of captopril , quinapril and placebo on blood pressure , urinary excretion of 2,3-dinor-6-keto-PGF1 alpha , and the vasodepressor response to i.v . bradykinin in 21 salt-replete normal-to-high renin hypertensive patients . Captopril and quinapril doses were titrated to lower pressure similarly . Captopril , but not quinapril , increased excretion of prostacyclin metabolite ( 217 +/- 50 vs. 135 +/- 21 pg/mg Cr base line , P < .05 ) . Both ACE inhibitors dramatically , equally potentiated the vasodepressor response to bradykinin ; the bradykinin dose required to decrease mean arterial pressure 15 mm Hg or increase pulse 20 bpm was 50-fold lower in ACEI-treated than in placebo-treated subjects ( 10 +/- 0 and 12.1 +/- 2.1 ng/kg/min in captopril and quinapril groups vs. 567 +/- 109 ng/kg/min in the placebo group ; P < .005 ) . ACE inhibition significantly attenuated the prostacyclin response to bradykinin at any given level of hypotensive response . Indomethacin abolished the prostacyclin response to bradykinin but did not alter the vasodepressor response . These data demonstrate that ACE inhibitors potentiate bradykinin-mediated vasodepression through a prostaglandin-independent mechanism . They suggest that although ACE inhibitors increase prostaglandins by increasing bradykinin , ACE inhibitors may attenuate prostaglandin production through a second bradykinin-independent mechanism .
88696
Intervention_Physical
angiotensin converting enzyme inhibitors
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Intervention_Pharmacological
bradykinin .
88698
Intervention_Physical
Angiotensin converting enzyme ( ACE )
88699
Intervention_Physical
ACE
88700
Intervention_Physical
ACE inhibitors
88701
Intervention_Physical
ACE inhibitors
88702
Intervention_Physical
ACE inhibitors
88703
Intervention_Physical
ACE
88704
Intervention_Pharmacological
captopril , quinapril
88705
Intervention_Control
placebo
88706
Intervention_Pharmacological
bradykinin
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Intervention_Pharmacological
Captopril and quinapril
88708
Intervention_Pharmacological
Captopril
88709
Intervention_Physical
ACE
88710
Intervention_Physical
ACEI-treated
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Intervention_Control
placebo-treated
88712
Intervention_Pharmacological
captopril
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Intervention_Pharmacological
quinapril
88714
Intervention_Control
placebo
88715
Intervention_Physical
ACE
88716
Intervention_Pharmacological
Indomethacin
88717
Intervention_Physical
ACE
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Outcome_Physical
prostacyclin metabolite
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Outcome_Physical
vasodepressor response
88720
Outcome_Physical
mean arterial pressure
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Outcome_Physical
prostacyclin response to bradykinin
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Outcome_Other
prostacyclin response
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Outcome_Other
vasodepressor response .