Relevance of Blockade of Cardiac and Circulatory Angiotensin-Converting Enzyme for the Prevention of Volume Overload–Induced Cardiac Hypertrophy

Abstract

The present findings further stress the involvement of the renin-angiotensin system as a trophic stimulus in the development of cardiac hypertrophy in this model. Moreover, the low affinity of enalapril for cardiac ACE appears to lead to continuous angiotensin II generation in the heart and can thus explain the failure of enalapril to attenuate hypertrophic response of the heart induced by shunt despite decreasing cardiac volume overload.