Coronary resistance arteriolar diameter importantly regulates myocardial blood flow, and is influenced by circulating neurohumoral agents. Angiotensin II (A-II) is a circulating polypeptide that is chronically elevated in heart failure and serves as a potent peripheral vasoconstrictor agent. However, its effects on isolated coronary resistance arterioles is relatively unknown. We compared the vasomotor effects of A-II on coronary epicardial and resistance arterioles in vitro from both the canine and porcine heart in order to determine the effects of A-II in different vascular beds and species. Epicardial rings were studied under isometric recording conditions, while resistance arterioles (50–150 µm) were studied in vitro using a video imaging system to record diameter. A-II, whether applied to passively distended or preconstricted porcine resistance arterioles, did not cause vasoconstriction when applied as a bolus or as cumulative doses. In preconstricted canine resistance arterioles, A-II elicited dose-dependent vasodilation (EC<sub>50</sub> = 0.2 n M) . In passively distended canine arterioles, high concentrations of A-II (0.1 µ M)applied as a bolus elicited transient vasoconstriction in 28% of the vessels studied. In large epicardial rings, A-II was a weak vasoconstrictor, with greater potency in canine arteries compared to porcine arteries. In canine arteries, vasoconstriction to A-II was augmented after incubation with indomethacin. In contrast to the findings in canine arteries, the A-II vasoconstrictor response in porcine coronary arteries was decreased after incubation with indomethacin or removal of the endothelium. Thus, A-II elicits the release of a vasodilator prostanoid in epicardial canine coronary arteries and a vasoconstrictor prostanoid in porcine vessels which modulate the vasomotor action of A-II. Receptor binding assays to compare A-II receptors in resistance arterioles and epicardial arteries showed that porcine arterioles possessed significantly more membrane receptors for A-II than porcine epicardial vessels, whereas there was no difference between canine epicardial and arteriolar A-II receptor densities. In conclusion, A-II exerted complex actions on both large epicardial vessels and resistance arterioles, with significant differences between species. A-II was a weak vasoconstrictor in both porcine and canine epicardial vessels. The net vasomotor response was the result of interactions between vasoactive prostanoids and direct smooth muscle vasoconstrictor effects on the coronary artery. A-II was a potent vasodilator of canine, but not porcine, resistance arterioles, and in some vessels elicited transient vasoconstriction at high A-II concentrations. Despite the presence of A-II receptors, in porcine resistance arterioles A-II had no vasomotor effects in either passively distended or preconstricted arterioles.