Brain or B-type natriuretic peptide(BNP) is an endogenous 32 amino acid polypetide hormone. BNP initially was first isolated from porcine brain by Sudoh et al., but more recently it has been found to be secreted mainly by the ventricular myocardium in response to volume and pressure overload. Plasma concentrations of BNP are increased in patients with congestive heart failure and are closely correlated to both of clinical manifestation and hemodynamic status. BNP has a spectrum of biological actions including diuretic, natriuretic, smooth muscle relaxant, inhibiting myocardial fibrotic responses, and suppressing rennin-angiotensin-aldosterone axis and sympathetic nervous system secondary to heart failure. Patients with congestive heart failure are in a state of resistance to endogenous BNP, probably because of the increased expression of the clearances receptors or the increase of degradative endopeptidase activity and so on. That is, endogenous BNP levels in patients with heart failure are insufficient to compensate these pathophysiologic changes. Recombinant human brain natriuretic peptide(rhBNP) is a produced peptide, upon biologic recombinant technic, that is structurally identical to BNP secreted from the human heart. Recent evaluation of rhBNP in the treatment of acute decompensated heart failure(ADHF) has demonstrated significant symptom improvement, in association with decreased preload and afterload and increased cardiac output, without a proarrhythmic effect. 2001 witnessed the first approval by the Food and Drug Administration(FDA) of a drug, rhBNP, for ADHF in nearly 15 years and was defined as a new class of drug.Persistent and serious ischemia may contribute to large and rapid cardiac...
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