Ren L M, Nakane T, Chiba S
Department of Pharmacology, Shinshu University School of Medicine, Matsumoto, Japan.
Eur J Pharmacol. 1996 Jan 4;295(1):61-8. doi: 10.1016/0014-2999(95)00654-0.
Vasoconstrictions induced by periarterial electrical stimulation were analysed pharmacologically in the canine isolated perfused splenic artery. Phentolamine enhanced the vasoconstrictions at 1 Hz but inhibited those at 10 Hz. Suramin and P2x purinoceptor desensitization with alpha,beta-methylene ATP abolished the phentolamine-enhanced and -resistant vasoconstrictions. alpha,beta-Methylene ATP inhibited the vasoconstrictions at 1 Hz and by exogenous ATP but did not change those at 10 Hz and by exogenous noradrenaline. Suramin reduced the vasoconstrictions by the electrical stimulations and alpha,beta-methylene ATP but did not affect those by exogenous ATP. Prazosin did not affect the vasoconstrictions at 1 Hz but inhibited those at 10 Hz. Rauwolscine enhanced the prazosin-resistant vasoconstrictions. These results suggest that the electrical stimulation at 1 Hz releases purinergic transmitters (ATP or a closely related compound) as a dominant candidate for the vasoconstrictions, and a co-released noradrenaline may inhibit the release of purinergic transmitters through presynaptic alpha 2-adrenoceptors in the canine splenic artery.
在犬离体灌注脾动脉中，对动脉周围电刺激诱导的血管收缩进行了药理学分析。酚妥拉明在1Hz时增强血管收缩，但在10Hz时抑制血管收缩。苏拉明和用α,β-亚甲基ATP使P2x嘌呤受体脱敏消除了酚妥拉明增强和抵抗的血管收缩。α,β-亚甲基ATP在1Hz时抑制血管收缩以及外源性ATP诱导的血管收缩，但不改变10Hz时以及外源性去甲肾上腺素诱导的血管收缩。苏拉明减少电刺激和α,β-亚甲基ATP诱导的血管收缩，但不影响外源性ATP诱导的血管收缩。哌唑嗪不影响1Hz时的血管收缩，但抑制10Hz时的血管收缩。育亨宾增强哌唑嗪抵抗的血管收缩。这些结果表明，1Hz的电刺激释放嘌呤能递质（ATP或密切相关的化合物）作为血管收缩的主要候选递质，并且共同释放的去甲肾上腺素可能通过犬脾动脉中的突触前α2-肾上腺素受体抑制嘌呤能递质的释放。
