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Abstract
he natriuretic peptide family consists of famous three endogenous ligands; atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP), and is involved in the regulation of cardiovascular homeostasis, induce vasodilatation, increase diuresis, and inhibit rennin and aldosterone production and thus are important regulators of the fluid and electrolyte homeostasis of the body.
The natriuretic peptides share a common structure. There is a 17-amino acid disulfide-bonded ring with N-terminal and C-terminal arms of various lengths and sequences. In the ring, 11 amino acids are conserved among the natriuretic peptides.
BNP may act as a compensating mechanism in cardiovascular diseases in order to reduce preload. However, the increase in endogenous BNP is often not sufficient to compensate for volume overload in diseases like established hypertension and heart failure. The therapeutic benefits of BNP infusion are most clear in patients with heart failure, although the hemodynamic effects of BNP appeared to be dependent on the dose.
Brain natriuretic peptide (BNP) levels are simple and objective measures of cardiac function. These measurements can be used to diagnose heart failure, including diastolic dysfunction, and using them has been shown to save money in the emergency department setting. The high negative predictive value of BNP tests is particularly helpful for ruling out heart failure.
Over the last decade brain natriuretic peptide (BNP) emerged as a cardiac hormone of clinical interest in diagnosis, prognosis and treatment of patients with Heart Failure (HF). The diagnostic potential of BNP is now well established both in patients with suspected HF as well as in patients with asymptomatic left ventricular systolic dysfunction. The prognostic information obtained from BNP levels in HF and acute myocardial infarction patients seems even more promising.