Natriuretic peptides: Physiological, pathophysiological and clinical aspects

Abstract

A milestone was reached in cardiophysiology when in 1981 DeBold demonstrated that the heart functions as an endocrine gland by injecting an extract of atrial muscle into rats, resulting in an induction of natriuresis and a drop in blood pressure. This observation then led to the discovery of a family of related peptides with slightly different amino acid compositions working in concert to achieve the maintenance of sodium and volume homeostasis. The natriuretic peptide family consists of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP), and Urodilatin (URO) with their tissue-specific distribution including the heart (ANP, BNP), brain (ANP, BNP, CNP), endothelial cells (CNP), and kidney (URO). These peptides were thought to be primarily involved in cardiovascular and renal functions but have now proven to play a role in other physiological systems. In view of their known biological effects, therapeutic efficacy from administration of ANP, BNP or URO might be anticipated, for example in acute renal failure or congestive heart failure. A number of clinical trials suggest that application of these peptides may represent a new pharmacological tool in the treatment or prevention of these diseases, but the clinical benefit still needs to be shown in large controlled studies. In addition to therapeutic options it is possible that plasma concentrations of ANP and BNP could play a role as diagnostic and prognostic markers of cardiac dysfunction.