Kawai Y, Ohhashi T, Azuma T
Nihon Heikatsukin Gakkai Zasshi. 1981 Sep;17(3):131-6.
Adenosine triphosphate (ATP) has been known to induce vasodilation in various vascular beds. Recently, we reported that ATP produced vasoconstrictions in isolated internal and external carotid arteries of dogs. In the present study, the mode of the ATP-induced vasoconstriction in the internal carotid artery was analysed from the physiological and pharmacological points of view. The results obtained were as follows: 1) ATP (5 X 10(-6) approximately 2 X 10(-4) M) caused dose-dependent vasoconstrictions in the internal carotid artery. 2) The ATP-induced vasoconstriction was not affected by pretreatment with phenoxybenzamine, propranolol, atropine, cyproheptadine, or tetrodotoxin. 3) Verapamil suppressed dose-dependently the contractile response. 4) ATP caused no vasoconstriction in a calcium-free Krebs solution containing Im M EGTA. 5) ATP produced no further vasoconstriction in the preparation which had been in a state of contracture in a high potassium Krebs solution. These results suggest that an increase of potential-dependent Ca++ influx into the arterial smooth muscle cells may play a major role in the ATP-induced vasoconstriction.
已知三磷酸腺苷(ATP)可在各种血管床中诱导血管舒张。最近,我们报道ATP在犬离体颈内动脉和颈外动脉中可引起血管收缩。在本研究中,从生理学和药理学角度分析了ATP诱导颈内动脉血管收缩的方式。获得的结果如下:1)ATP(5×10⁻⁶至2×10⁻⁴M)在颈内动脉中引起剂量依赖性血管收缩。2)ATP诱导的血管收缩不受苯氧苄胺、普萘洛尔、阿托品、赛庚啶或河豚毒素预处理的影响。3)维拉帕米剂量依赖性地抑制收缩反应。4)在含有1mM乙二醇双四乙酸(EGTA)的无钙 Krebs 溶液中,ATP不引起血管收缩。5)在高钾Krebs溶液中处于挛缩状态的制剂中,ATP不会进一步引起血管收缩。这些结果表明,电压依赖性Ca²⁺流入动脉平滑肌细胞的增加可能在ATP诱导的血管收缩中起主要作用。