Stutzin A, Paravic F, Ormenño G, Orrego F
Mol Pharmacol. 1983 Mar;23(2):409-16.
The blocking effects of guanethidine on electrically induced, neurally mediated, contractions of the guinea pig vas deferens in vitro could be markedly antagonized by the bee venom polypeptide apamin (20-60 nM), by 0.1 mM methylene blue, and (less regularly) by 0.1-0.15 mM quinine, three substances known to inhibit calcium-activated potassium conductance in a variety of cells. Guanethidine (20 microM) was also found to inhibit (by 88%) the release of [3H]norepinephrine induced by electrical stimulation (20-Hz, 2-msec, biphasic pulses of supramaximal voltage). Such inhibition was decreased to 39% when 20 nM apamin was present together with guanethidine, thus showing that the effect of this polypeptide is presynaptic. On the basis of these findings, we suggest that guanethidine may block adrenergic neurons by activating their calcium-activated potassium conductance, presumably by releasing intracellular calcium.
在体外，蜂毒多肽蜂毒明肽（20 - 60 nM）、0.1 mM亚甲蓝以及（不太规律地）0.1 - 0.15 mM奎宁（已知这三种物质可抑制多种细胞中钙激活钾电导）可显著拮抗胍乙啶对豚鼠输精管电诱导的、神经介导的收缩的阻断作用。还发现胍乙啶（20 μM）可抑制（88%）电刺激（20 Hz，2毫秒，超最大电压双相脉冲）诱导的[3H]去甲肾上腺素释放。当20 nM蜂毒明肽与胍乙啶同时存在时，这种抑制作用降至39%，表明该多肽的作用是突触前的。基于这些发现，我们认为胍乙啶可能通过激活其钙激活钾电导来阻断肾上腺素能神经元，推测是通过释放细胞内钙来实现的。
