Brain Natriuretic Peptide (1-32), rat acetate (BNP (1-32), rat acetate) is a 32 amino acid polypeptide hormone synthesized by ventricular cardiomyocytes as a result of myocardial cell stretching (cardiomyocyte distension)[1].

B-type natriuretic peptide (BNP) combats cardiac stress by reducing blood pressure and ventricular fibrosis. Rat BNP BNP (1-32) (rBNP (1-32)) is an amino-truncated form of the 45 residue natural rat form of BNP[1]. Atrial natriuretic peptide-(1-28) (ANP), brain natriuretic peptide-(1-32) (BNP) and C-Type natriuretic polypeptide (CNP) occur in the brain, are concentrated in the anteroventral area of the third cerebral ventricle and participate in the regulation of body fluid homeostasis. The ANP(1-28), BNP (1-32) and CNP(1-32) function in the mammalian brain to regulate salt and water homeostasis via their receptors NPR-A and NPR-B[2].

The depressor, natriuretic and cyclic GMP responses to several species of brain natriuretic peptide (BNP) are compared to atrial natriureticpeptide (ANP) 99-126 in conscious spontaneously hypertensive rats (SHR) and in conscious cynomolgus monkeys treated with vehicle or the selective neutral endopeptidase inhibitor SQ 28603. In the conscious SHR, the natriuretic and cyclic GMP responses to 3 nmol/kg i.v. rat BNP (1-32) greater than rat ANP 99-126 greater than pig BNP-26 and sre significantly potentiated by 100 mumol/kg i.v. SQ 28,603. Human BNP-32 is inactive in the SHR treated with either vehicle or SQ 28,603. In contrast, 1 nmol/kg i.v. of human BNP (1-32) stimulates renal and depressor responses in the conscious monkeys that are greater than or equal to those elicited by human ANP 99-126, whereas 3 nmol/kg i.v. rat BNP (1-32) reduces mean arterial pressure without affecting renal function[3].