Angiotensin II's influence on circulating levels of prostaglandin I2 metabolite 6-keto-PGF1-alpha were determined during a pharmacological stress test of left ventricular function in 10 control subjects and 5 patients with coronary artery disease. Angiotensin II infusion (1.5 +/- 0.34 micrograms/min) led to a significant increase of mean arterial blood pressure in both study groups (p less than 0.001). Heart rate decreased in control subjects (p less than 0.01) whereas in patients with coronary artery disease no significant change occurred. Global left ventricular ejection fraction determined by gated blood pool scanning decreased significantly in both study groups (p less than 0.05). The lack of reflex bradycardia in patients with coronary artery disease may be due to a compensatory increased sympathetic tone, prohibiting a more pronounced decline in ejection fraction. 6-keto-PGF1-alpha levels could be measured only in 6 of 15 persons. In the others they were below the limit of detection of the assay (70 pg/ml). During angiotensin II infusion 6-keto-PGF1-alpha increased significantly and could be determined in all persons. Patients with coronary artery disease reached slightly higher 6-keto-PGF1-alpha levels than controls (119 +/- 19 pg/ml versus 91.5 +/- 7 pg/ml; n.s.). Thus although angiotensin II infusion leads to vasoconstriction and increases peripheral resistance it also stimulates the production of vasodilating prostaglandins which may play a role in preserving microcirculation.