The current study examines the prostaglandin contribution to angiotensin II-induced vasoconstriction in isolated perfused cat arteries. Superior mesenteric arteries were the most sensitive to angiotensin II. Superior mesenteric arteries responded to angiotensin II (25 nM) with a vasoconstriction which increased perfusion pressure 47 mm Hg. Sodium meclofenamate diminished this response to 2 mm Hg, but indomethacin did not significantly attenuate this effect. Angiotensin II (25 nM) produced a 31 mm Hg increase in perfusion pressure in coronary arteries but indomethacin (20 µM) or sodium meclofenamate (75 µM) reduced this response to 11 and 14 mm Hg, respectively (p < 0.05). Hepatic arteries were the least responsive to angiotensin. Also, neither cyclooxygenase inhibitor reduced the angiotensin II response in the common hepatic artery. Angiotensin II, therefore, may require prostaglandin synthesis for part of its vasoconstrictor activity in certain vascular beds, notably the coronary vasculature, but less so in splanchnic arteries.