Effects of angiotensin converting enzyme 2 and angiotensin converting enzyme genes on cardiac remodeling in rats with heart failure

Abstract

To investigate the effects of angiotensin converting enzyme 2 and angiotensin converting enzyme genes on the cardiac remodeling process in heart failure rats. 38 rats were randomly divided into sham-operated group (S group), heart failure group (H group) and heart failure exercise group (HE group). An incremental load exercise test was used to determine the maximum running speed of the HE group, while the S and H groups maintained their daily activities. The cardiac structure and function and the pathological changes were compared. Compared with S group, body weight, left ventricular internal diameter at diastole, fractional shortening, left ventricular ejection fraction, myocytes and angiotensin converting enzyme/ angiotensin converting enzyme 2 ratio were decreased while left ventricular weight, left ventricular mass index, ventricular anterior wall diameter at diastole, left ventricular anterior wall diameter at systole, left ventricular posterior wall diameter at diastole, left ventricular posterior wall diameter at systole, atrial natriuretic factor, angiotensin-I, angiotensin-II, messenger RNA and angiotensin converting enzyme, angiotensin converting enzyme 2, transforming growth factor beta protein levels and collagen fibers (i.e. collagen volume fraction) were increased in H group (p<0.05). Compared with H group, left ventricular weight, left ventricular mass index, left ventricular internal diameter at diastole, fractional shortening, left ventricular ejection fraction, myocytes were increased while collagen volume fraction, atrial natriuretic factor, angiotensin-I, angiotensin-II, messenger RNA and angiotensin converting enzyme, angiotensin converting enzyme 2, transforming growth factor beta protein levels were reduced and angiotensin converting enzyme/angiotensin converting enzyme 2 ratio were decreased (p<0.05). Long-term aerobic exercise attenuated myocardial fibrosis and improved cardiac function by inhibiting collagen synthesis and promoting its degradation and cardiac remodeling was inhibited and improved by a mechanism that may be related to partial restoration of angiotensin converting enzyme 2/angiotensin converting enzyme signalling function.