Fifteen patients had left ventricular function measured by the angiotensin infusion method. Seven patients had no evidence of heart disease, and eight patients had angina pectoris and coronary arteriographic evidence of coronary disease without congestive heart failure. During angiotensin infusion, those patients without heart disease had a decrease in cardiac index (average, 0.63 L. per minute per square meter) and a decrease in heart rate (average, 12 beats per minute.) The ventricular function curve had a poor SWI response in four of the seven subjects. The patients with coronary artery disease also had a reduction in cardiac index during angiotensin (average, 0.44 L. per minute per square meter) and the heart rate was unchanged in four subjects, increased in two subjects, and decreased in two subjects. Six of the subjects had flat or descending slopes on the function curve, and in one subject there was only a very gradual ascending slope. Many of the curves of both groups looked similar so that the function curves did not differentiate between those patients with or without heart disease. The mechanism for production of bradycardia, reduction of cardiac output, and depressed function curves with angiotensin is multifactorial, but is probably due to the baroreceptor reflex response, the increase in coronary artery resistance, and possible to the direct effect of increased left ventricular afterload itself. The ventricular response to angiotensin is so variable that the angiotensin infusion method of evaluating ventricular function is not reliable.