Sato H, Ohizumi Y, Hikino H
Eur J Pharmacol. 1979 Apr 1;55(1):83-92. doi: 10.1016/0014-2999(79)90150-x.
Mesaconitine (MA) caused contraction of the isolate guinea pig vas deferens in a dose-dependent manner (3 x 10(-6) - 10-(-4) g/ml) and nonspecifically potentiated the contractile response to norepinephrine (NE), acetylcholine, histamine and tyramine. Tachyphylaxis developed during the repeated application of MA. The contraction produced by MA was prevented by treatment with phentolamine, phenoxybenzamine, procaine, bretylium or tetrodotoxin, pretreatment with reserpine or 6-hyroxydopamine, or denervation. Atropine or hexamethonium did not abolish the effect of MA, excluding the possibility that the muscarinic and nicotinic receptors are the site of action of MA. MA elicited a dose-dependent release of NE from the isolated vas deferens which had been blocked by treatment with tetrodotoxin, pretreatment with reserpine, or the exclusion of calcium ion from the bath medium. Consequently, it is concluded that MA-induced contraction was brought about by the release of NE from pre-synaptic neuronal sites and by excitation of the post-synaptic membrane.
中乌头碱（MA）以剂量依赖性方式（3×10⁻⁶ - 10⁻⁴ g/ml）引起离体豚鼠输精管收缩，并非特异性地增强对去甲肾上腺素（NE）、乙酰胆碱、组胺和酪胺的收缩反应。重复应用MA时会出现快速耐受性。MA产生的收缩可通过酚妥拉明、酚苄明、普鲁卡因、溴苄铵或河豚毒素处理、利血平或6-羟基多巴胺预处理或去神经支配来预防。阿托品或六甲铵不能消除MA的作用，排除了毒蕈碱和烟碱受体是MA作用位点的可能性。MA引起离体输精管中NE的剂量依赖性释放，这种释放已被河豚毒素处理、利血平预处理或从浴液介质中排除钙离子所阻断。因此，得出结论，MA诱导的收缩是由突触前神经元部位释放NE和突触后膜兴奋引起的。
