MYOCARDIAL HYPERTROPHY, ANGIOTENSIN, AND ACE-INHIBITORS

The renin-angiotensin system has long been known as a potent determinant of cardiovascular homeostasis and a powerful regulator of vascular hemodynamics. Over the last twenty years, it has become clear that components of the renin-angiotensin system are present in and, in many instances, synthesized in local tissues. The role of some of these local renin systems is now becoming clear, but the role, if any, of local production of angiotensin II in the heart and vasculature remains unknown. Recent evidence indicates that angiotensin II can serve as a growth factor for a variety of cell types including those in the cardiovascular system, and it thus appears possible that systemically or locally produced angiotensin II could subserve important functions in the determination of heart and vasculature structure. Clinical studies tend to corroborate this possibility. The potent effects of converting enzyme inhibition on the regression of left ventricular hypertrophy, the demonstration that the administration of these agents following myocardial infarction reduces detrimental cardiac remodeling, and the finding that concerting enzyme inhibition prolongs survival in congestive heart failure patients all point to an important role of angiotensin II on cardiovascular function and raise the distinct possibility that angiotensin II growth effects are involved in these beneficial responses. Additionally, recent data demonstrate conclusively that under certain circumstances and in certain cell types locally produced angiotensin II can serve as an autocrine growth regulatory factor, further adding support to the idea that local renin systems may play an important role in the determination of cardiovascular structure.