심근비후에 의한 Natriuretic Peptides 유전자 표현에 대한 연구

Abstract

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are hormones secreted from the heart, and their plasma levels have been shown to be increased in patients with congestive heart failure (CHF). However, the precise mechanism for secretion of ANP and BNP are not known in CHF. This study was designed to determine the mechanisms regulating the increased levels of ANP and BNP gene expression in response to cardiac hypertrophy induced by isoproterenol (5 mg/kg, ip, for 5 days) in rats. The increased levels of ANP and BNP were investigated by RT-PCR method in the right atria and the left ventricles of hypertrophic hearts of rats. The extent of elevated expressions of ANP and BNP mRNA were more prominent in the left ventricles than those of the right atria. The increased expressions of ANP and BNP mRNA in the right atria were not inhibited by propranolol and clonidine, but those of ANP and BNP mRNA in the left ventricles were inhibited markedly by propranolol, clonidine, and metoprolol. Regarding the renin angiotensin system (RAS) on the ANP and BNP gene expressions, saralasin inhibited the increased levels of ANP and BNP mRNA in both the right atria and the left ventricles of the hypertrophic hearts, but captopril did not attenuate the elevated levels of the ANP and BNP gene expression. These findings suggest that the patterns of ANP and BNP gene expression provide better evidences for a pathologic condition of left ventricle than of right atrium. The underlying mechanisms of the observed ANP and BNP gene expression might be controlled by sympathetic system and RAS, mediated by angiotensin II from cardiac and extracardiac origin.