The renin-angiotensin system (RAS) is integrally involved in cardiovascular homeostasis (59). The principal mediator of the physiological actions of the RAS is the octapeptide angiotensin II (All). Angiotensinogen, the precursor of All, is hydrolyzed by the enzyme renin, thus resulting in the formation of the decapeptide angiotensin I (AI). The two carboxy terminal amino acids of AI are cleaved by angiotensin-converting enzyme (ACE) to form the octapeptide All (63). Angiotensin II directly modulates cardiac function as evidenced by effects on myocardial contractility and metabolism, and hypertrophic growth (5, 7, 17, 18, 22, 35, 46). The indirect cardiac effects of All include central nervous system actions such as stimulation of thirst and sympathetic outflow, stimulation of aldosterone synthesis and release, de creased renal excretion of sodium, and maintenance of vascular tone (4). The clinical relevance of the cardiac RAS is indicated by the beneficial effects of ACE inhibitors, which block the conversion of AI to All, in several patholog ical conditions (11, 31, 39, 41). Angiotensin-converting enzyme inhibition improves symptoms of congestive heart failure and reduces mortality in patients with this pathological condition (39). In acute myocardial infarction,