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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 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.