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Plasma concentrations of brain natriuretic peptide: will this new test reduce the need for cardiac investigations?

Atrial natriuretic peptide (ANP) was sequenced in 1984. The discovery ofANP led inevitably to a search for other peptides with natriuretic activity. In 1988 brain natriuretic peptide (BNP) and in 1990 C-type natriuretic peptide (CNP) were identified.12 ANP, BNP, and CNP are structurally similar but only 12 amino acids are common to all three peptides out of a total of 28 amino acids for ANP, 32 for BNP, and 22 for CNP. Though both BNP and CNP were originally identified in the porcine brain, concentrations of BNP are much higher in the heart than in the brain. The name "brain" natriuretic peptide is therefore absurd and there is a commendable tendency among the Japanese to re-name it B-type natriuretic peptide. Normally ANP is stored in large concentrations in the atria with much less in the ventricles whereas BNP is derived to a much greater extent from the cardiac ventricles. The ventricles secrete a large amount of BNP though they store only a small quantity. Plasma concentrations of ANP are usually higher than plasma concentrations of BNP, but in cardiac failure BNP concentrations increase much more than ANP concentrations-so that in severe heart failure plasma BNP often exceeds plasma ANP.3 This differential release rate may make BNP concentrations a more sensitive indicator of left ventricular dysfunction than ANP concentrations. The biological effects of ANP and BNP are very similar. They both cause natriuresis and vasodilatation and they both release cyclic guanosine monophosphate (GMP) and suppress aldosterone. Both are broken down by neutral endopeptidase.4 There are orally available inhibitors of neutral endopeptidase. These drugs increase BNP and ANP and it is probably because they increase both peptides that they are so potently natriuretic in heart failure. ANP but possibly not BNP is also cleared by unusual receptors called clearance receptors that bind the ANP but produce no biological effects, that is, they seem to mop up vast quantities of ANP. This seems a most curious function for these receptors but so far there is no better explanation for their role. One of the great hopes for ANP was that it could be infused in heart failure to produce a natriuresis. ANP does cause a natriuresis in heart failure, but unfortunately not to the same extent as in healthy people. This may be due to concurrent antinatriuretic influences in heart failure such as angiotensin II or noradrenaline or it could be because ANP renal receptors are downregulated. Yoshimura et al found that infused BNP had the opposite effect to ANP in that the natriuretic response to BNP