Actions of prostaglandins on isolated perfused cat coronary arteries

Effects of prostaglandins on coronary arterial smooth muscle were studied in isolated perfused cat coronary arteries. This preparation was shown to be responsive to known vasoactive agents, including angiotensin II, adenosine, and norepinephrine. Prostaglandins E2 and F2 alpha (PGE2 and PGF2 alpha) produced dose-dependent coronary arterial constriction at concentrations of 3 times 10(-9) M or greater. PGE1 produced a biphasic dose-response curve with constriction at low concentrations greater than 10(-7) M.PGI2 dilated coronary arteries at concentrations greater than 10(-8) M. Inhibition of endogenous prostaglandin synthesis with meclofenamate potentiated responses to prostaglandins. The endoperoxide, PGH2, slightly constricted cat coronary arteries. However, in the presence of human platelet microsomes, PGH2 was converted to thromboxane A2(TxA2), which was the most potent coronary artery constrictor among the naturally occurring compounds studied. Analysis of coronary artery perfusate for TxB2 confirmed the thromboxane generation, which was markedly lower in the presence of imidazole. Two synthetic endoperoxide analogs produced potent coronary arterial constriction. Induction of hypoxia to a PO2 of 50 mmHg or increasing basal tome with 30 mM KCl did not diminish coronary artery response to prostaglandins, suggesting that prostaglandins released from ischemic myocardial tissue may influence coronary arterial tone.