Clinical application of the natriuretic peptides in heart failure

The natriuretic peptides are a family of peptides each with a 17 amino acid disulphide ring structure, but are genetically distinct with diverse actions in cardiovascular, renal, and endocrine homeostasis. In humans, the family consists of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) of myocardial cell origin, C-type natriuretic peptide (CNP) is of endothelial origin, and urodilatin (Uro) is thought to be derived from the kidney. Furthermore, natriuretic peptides have also been isolated from a range of other vertebrates. Notably, some were found in snake venoms: Dendroaspis angusticeps natriuretic peptide was detected in the venom of Dendroaspis angusticeps (the green mamba); CNP analogues were also cloned from the venom glands of snakes of the Crotalinae subfamily; Pseudocerastes persicus natriuretic peptide, isolated from the venom of the Iranian snake Pseudocerastes persicus and three natriuretic-like peptides (TNP-a, TNP-b, and TNP-c) isolated from the venom of Oxyuranus microlepidotus. Human recombinant ANP (Carperitide) has been approved for the clinical management of acute decompensated CHF in Japan since 1995, human recombinant BNP (Nesiritide) has been approved for the same clinical indication in the USA since 2001, and human recombinant Uro (Ularitide) is currently undergoing phase III clinical trails in Europe. As biomarkers, both BNP and NT-pro BNP are currently used clinically to aid the diagnosis of CHF, assessing the severity of CHF and risk stratification in patients with coronary artery diseases. In this review, we will attempt to provide an update on important issues regarding natriuretic peptides in CHF.