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

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 alpha,beta-methylene ATP > 2-methylthio ATP > UTP > ATP. That for vasodilation was ATP > 2-methylthio ATP > alpha,beta-methylene ATP >> UTP in the preparations precontracted by 20 mM KCl. Aminophylline inhibited the vasodilation induced by adenosine, but not that induced by ATP. Alpha,beta-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 P2X purinoceptors on the smooth muscle and vasodilation via P2Y purinoceptors on the endothelium through mainly the release of nitric oxide in the canine coronary artery, respectively.