Current data support the existence of an endogenous renin-angiotensin system in the heart. Vascular angiotensin may contribute to the regulation of coronary vascular tone. Enhanced local angiotensin production in areas of vascular injury or inflammation may result in increased vasoconstriction or vasospasm. Cardiac angiotensin may adversely influence myocardial metabolism and provoke ventricular arrhythmia during ischemia and reperfusion-induced myocardial injury. Local angiotensin may stimulate cardiac contractility. In addition, angiotensin may influence cardiac myocyte growth and may contribute to the development of cardiac hypertrophy in hypertension. Recent data show that the pharmacologic inhibition of cardiac angiotensin converting enzyme may have important therapeutic consequences for the ischemic, hypertrophic, or failing heart.