Natriuretic peptides in cardiac and renal failure

linkage essential for receptor binding. ANP and BNP are cardiac hormones mainly secreted from the atrium and the ventricle respectively, whereas CNP is of endothelial origin. ANP and BNP bind to the natriuretic peptide A-receptor (NPR-A) and mediate the biological actions of natriuresis, vasodilatation and renin inhibition. In contrast, CNP lacks renal actions but causes vasodilatation via binding to the NPR-B. Because of their utmost significance as diagnostic and prognostic parameters, this article will focus on B-type natriuretic peptides. The B-type natriuretic peptide is synthesised in cardiac myocytes as a 134 amino acid pre-pro hormone, which is subsequently cleaved to yield a 108 amino acid pro-peptide that is stored in secretory granules within the myocytes. In response to the appropriate stimulus, pro-BNP is proteolytically cleaved into the biologically active mature BNP and the biologically inactive N-terminal (NT)-proBNP (76 amino acids), which are released into the blood stream (Figure 1). Although BNP is also produced in atrial tissue and in right ventricular myocardium, highest concentrations of BNP have been found in the myocardium of the left ventricle. The mature B-type natriuretic peptide is a 32-amino acid polypeptide hormone which is rapidly released by the ventricles of the heart in response to myocardial stretch. Upon release the neurohormone affects body fluid volume (through natriuresis and diuresis) and vascular tone (Figure 2). Since high ventricular filling pressure is a common feature in congestive heart failure (CHF), plus the fact that body fluid homeostasis and vascular tone play an essential role in the pathophysiology of CHF, BNP has been investigatedas a candidatemarker for cardiac neurohormonal activation in patients with CHF. Natriuretic peptides in cardiac and renal failure