The identification of natriuretic peptides as key regulators of natriuresis and vasodilatation, and the appreciation that their secretion is under the control of cardiac haemodynamic and neurohumoral factors, have boosted a wide interest among scientists and cardiologists in the last 10 years. Brain natriuretic peptide (BNP, 32 amino acids) is secreted into the circulation mainly by left ventricular (and atrial) myocytes in conditions of overload or wall stress (dilatation and/or abnormal filling pressure). Through its binding to specific membrane receptors (NPR-A), the hormone generates the second messenger cGMP and stimulates the nitric oxide system. BNP may be envisioned as a “good” hormone that counteracts the effects of the sympathetic and renin-angiotensin-aldosterone systems by favouring peripheral vasodilatation, renal excretion of water and sodium, and by inhibiting abnormal vascular cell growth.

The authors of this commentary share most of the views expressed in two recent editorials.1 2 Plasma BNP concentration rises with the severity of cardiac disease. An early report showed how the plasma BNP-like immunoreactive level was increased in patients with heart failure as a function of New York Heart Association (NYHA) functional class.3 Since then, virtually all clinical, functional, and instrumental indexes of the severity of heart failure have been found to be related to circulating BNP …