Reilly M J, Hirst G D
Department of Zoology, University of Melbourne, Parkville, Australia.
J Auton Nerv Syst. 1996 Feb 5;57(1-2):93-100. doi: 10.1016/0165-1838(95)00105-0.
The responses to sympathetic nerve stimulation and to applied ATP in the guinea-pig vas deferens were compared. Nifedipine (10 microM) markedly reduced the non-adrenergic neural contraction but only partially blocked the contractions produced by bath-applied ATP. Suramin (300 microM) also markedly reduced the contractile responses produced by nerve stimulation, but had no significant effect on the contractions produced by bath-applied ATP. Using intracellular recording techniques, nerve stimulation was shown to produce an excitatory junction potential which was abolished by suramin (1 microM). Ionophoretic application of ATP and bath-applied ATP also produced a depolarization. Suramin (1 microM) failed to abolish the response to bath-applied ATP and enhanced the ionophoretically induced depolarization. These results suggest either that ATP is not a transmitter in the vas deferens or that two classes of purinoceptor are present, one suramin-sensitive receptor which produces a contraction via the opening of voltage-dependent Ca2+ channels, and another which is suramin-resistant and produces a contraction by another means.
比较了豚鼠输精管对交感神经刺激和应用ATP的反应。硝苯地平（10微摩尔）显著降低了非肾上腺素能神经收缩，但仅部分阻断了浴槽中应用ATP所产生的收缩。苏拉明（300微摩尔）也显著降低了神经刺激所产生的收缩反应，但对浴槽中应用ATP所产生的收缩没有显著影响。使用细胞内记录技术，显示神经刺激产生一种兴奋性接头电位，该电位被苏拉明（1微摩尔）消除。离子电泳应用ATP和浴槽中应用ATP也产生去极化。苏拉明（1微摩尔）未能消除对浴槽中应用ATP的反应，反而增强了离子电泳诱导的去极化。这些结果表明，要么ATP不是输精管中的递质，要么存在两类嘌呤受体，一类是对苏拉明敏感的受体，它通过电压依赖性Ca2+通道的开放产生收缩，另一类对苏拉明有抗性，通过另一种方式产生收缩。
