Clinical Information

B-type natriuretic peptide [BNP] is a 32 amino acid neurohormone secreted by the heart to regulate blood pressure and fluid balance (1). BNP is stored in and secreted predominantly from membrane granules in the heart ventricles and is continuously released from the heart in response to both ventricle volume expansion and pressure overload (2).

The renin-angiotensin and natriuretic peptide system counteract each other to regulate arterial pressure. When arterial pressure decreases, the kidneys release renin, a small protein enzyme that circulates throughout the bloodstream. Angiotensinogen, a polypeptide released from the liver, is cleaved in the circulation by renin to form angiotensin I. This biologically inactive decapeptide is cleaved in turn by a second enzyme (angiotensin converting enzyme) to form active angiotensin II. Angiotensin II acts as a vasoconstrictor to increase the peripheral resistance of the arterioles, which increases arterial pressure. Both BNP and ANP (atrial natriuretic peptide) are activated by atrial and ventricular distension due to increased intracardiac pressure. These peptides have both natriuretic and diuretic properties: they raise sodium and water excretion by increasing the glomerular filtration rate and inhibiting sodium reabsorption by the kidney. The natriuretic peptides counteract the effects of renin secretion, causing a reduction of blood pressure and in extracellular fluid volume (3).

The New York Heart Association (NYHA) developed a functional classification system for congestive heart failure (CHF) consisting of 4 stages based on the severity of the symptoms.
Various studies have demonstrated that circulating BNP concentrations increase with the severity of CHF based on the NYHA classification (4-6).