豚鼠肠系膜动脉中去甲肾上腺素能传递的调节：一项电生理研究。
Modulation of noradrenergic transmission in the guinea-pig mesenteric artery: an electrophysiological study.
作者信息
Kuriyama H, Makita Y
出版信息
J Physiol. 1983 Feb;335:609-27. doi: 10.1113/jphysiol.1983.sp014554.
We carried out electrophysiological experiments on guinea-pig mesenteric arteries in an attempt to clarify the modification of noradrenaline (NA) release from noradrenergic nerve terminals by the action of prejunctional adrenoceptors. NA (10(-7)-10(-5) M) suppressed the amplitude of the first excitatory junction potential (e.j.p.(f], the facilitation process, and the e.j.p. after facilitation was completed (e.j.p.(s]with no change in the post-junctional membrane properties of smooth muscles. These actions of NA on e.j.p.s were antagonized by high concentrations of extracellular Ca, [Ca]o, but not in a simple competitive manner. NA (10(-7) M) suppressed the appearance but not the amplitude of the miniature e.j.p.s. These effects of NA on transmission indicate that NA acts on prejunctional nerve terminals and suppresses the release of NA from nerve terminals rather than producing a desensitization of post-junctional adrenoceptors. Prazosin and phentolamine (10(-6) M) did suppress the NA-induced contraction (greater than 10(-6) M) but did not suppress the contraction evoked by perivascular nerve stimulation, below a frequency of 1.0 Hz. At a dose of 10(-7) M, yohimbine, clonidine, prazosin and phentolamine had no effect on the muscle membrane potential and resistance. Yet on the e.j.p.(f), yohimbine and clonidine caused suppression, phentolamine enhancement and prazosin had no effect. On the e.j.p.(s), yohimbine and phentolamine caused enhancement, clonidine suppression and prazosin had no effect. These results indicate that at least three different adrenoceptors are distributed on the neuromuscular junction in this tissue, i.e. alpha 1-extrajunctional, alpha 2-prejunctional, and an unknown subtype of intrajunctional adrenoceptors. Furthermore, the feedback mechanism on NA release is mediated by suppression of the influx of Ca. Nonselective and non-specific actions of alpha-adrenoceptor agonists and antagonists were also elucidated.
我们对豚鼠肠系膜动脉进行了电生理实验，试图阐明节前肾上腺素能受体的作用对去甲肾上腺素能神经末梢释放去甲肾上腺素（NA）的影响。NA（10⁻⁷ - 10⁻⁵ M）可抑制首个兴奋性接头电位（e.j.p.(f]）的幅度、易化过程以及易化完成后的e.j.p.（e.j.p.(s]），而平滑肌的节后膜特性无变化。NA对e.j.p.s的这些作用可被高浓度的细胞外钙[Ca]o拮抗，但并非以简单的竞争性方式。NA（10⁻⁷ M）可抑制微小e.j.p.s的出现但不影响其幅度。NA对传递的这些作用表明，NA作用于节前神经末梢，抑制神经末梢释放NA，而非使节后肾上腺素能受体脱敏。哌唑嗪和酚妥拉明（10⁻⁶ M）确实可抑制NA诱导的收缩（大于10⁻⁶ M），但在频率低于1.0 Hz时，不抑制血管周围神经刺激诱发的收缩。剂量为1⁻⁷ M时，育亨宾、可乐定、哌唑嗪和酚妥拉明对肌膜电位和电阻无影响。然而，对于e.j.p.(f)，育亨宾和可乐定引起抑制，酚妥拉明引起增强，哌唑嗪无影响。对于e.j.p.(s)，育亨宾和酚妥拉明引起增强，可乐定引起抑制，哌唑嗪无影响。这些结果表明，在该组织的神经肌肉接头处至少分布有三种不同的肾上腺素能受体，即α1-接头外、α2-节前和一种未知亚型的接头内肾上腺素能受体。此外，对NA释放的反馈机制是通过抑制钙内流介导的。α-肾上腺素能激动剂和拮抗剂的非选择性和非特异性作用也得到了阐明。
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