摘出イヌ冠状動脈におけるATPの作用
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The responses of canine coronary arteries to ATP, its analogues and UTP were investigated in isolated, cannulated and per fused preparations. ATP induced a dose-dependent vasoconstriction followed by a vasodilation. The rank order of potency for eliciting vasoconstriction was a, β-methylene ATP>2-methylthio ATP>UTP>ATP, which is consistent with that previously observed for P_<2X>-purinoceptors. The rank order of potency for vasodilation was ATP>2methylthio ATP> α,β-methylene ATP. UTP did not induce vasodilation. The Pi-purinoceptor antagonist aminophylline inhibited adenosine-induced vasodilations, but it did not affect those ATP-induced. The selective P_<2X>-purinoceptor-desensitizing agent α,β-methylene ATP inhibited ATP-induced vasoconstrictions, but it did not affect those UTP-induced. Reactive blue 2, a putative P_<2Y>-purinoceptor antagonist inhibited ATP-induced vasodilations but it did not affect vasoconstrictions. The non-selective P_2-purinoceptor antagonist suramin inhibited ATP-induced vasoconstrictions. Removal of the endothelium by an intraluminal bolus injection of saponin (1 mg) significantly inhibited ATP-induced vasodilations, but it did not affect vasoconstrictions. t that, in the canine coronary arteries: (1) ATP and its analogues cause vasoconstrictions via P_<2X>-purinoceptors and vasodilations via P_<2Y>-purinoceptors; (2) P_<2X>- and P_<2Y>-purinoceptors are located on the smooth muscle and on the endothelium, respectively; (3) ATP is not acting through breakdown to adenosine; (4) the vasoconstrictor responses to UTP might be mediated by a receptor distinct from the P_<2X>- and P_<2Y>-purinoceptors.
- 東京女子医科大学の論文
- 1996-11-25
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