Pharmacological analysis of responses to ATP in the isolated and perfused canine coronary artery

Abstract

Vascular responses of the isolated and perfused canine coronary artery to adenosine 5′-triphosphate (ATP) were analyzed pharmacologically. At basal perfusion pressure, ATP induced a vasoconstriction followed by a vasodilation dose-dependently. The potency order for vasoconstriction was α, β-methylene ATP>2-methylthio ATP>UTP>ATP. That for vasodilation was ATP>2-methylthio ATP> α, β-methylene ATP≫UTP in the preparations precontracted by 20 mM KCl. Aminophylline inhibited the vasodilation induced by adenosine, but not that induced by ATP. α, β-Methylene ATP and suramin inhibited the vasoconstriction induced by ATP. Reactive blue 2 inhibited the vasodilation induced by ATP, but not the vasoconstriction. Removal of the endothelium by saponin and l- N G-nitroarginine inhibited the vasodilation induced by ATP, but indomethacin did not. The results suggest that ATP induces vasoconstriction via P 2X purinoceptors on the smooth muscle and vasodilation via P 2Y purinoceptors on the endothelium through mainly the release of nitric oxide in the canine coronary artery, respectively.