Hedlund H, Andersson K E, Larsson B
J Auton Pharmacol. 1985 Sep;5(3):261-70. doi: 10.1111/j.1474-8673.1985.tb00127.x.
Electrical field stimulation of ring preparations of the epididymal (Ve) and prostatic (Vp) parts of the human isolated vas deferens produced contractions with similar frequency-dependence and appearance. The contractions of Ve, but not of Vp preparations were abolished by tetrodotoxin (10(-6)M). Noradrenaline (NA), phenylephrine, and methoxamine, but not clonidine induced repetitive, phasic contractions in both Ve and Vp preparations, and increased the amplitude of electrically induced responses. Clonidine concentration-dependently decreased electrically induced contractions in Ve preparations, but had no significant effects in Vp preparations. Phentolamine and prazosin abolished electrically induced contractions in Ve but not in Vp preparations. In Ve rings the contractions were increased by rauwolscine; no such effect was observed in Vp preparations. Isoprenaline, propranolol, acetylcholine and carbachol had no effects in the Ve or Vp preparations. Scopolamine and atropine reduced electrically induced responses. Clonidine decreased and rauwolscine increased the electrically induced release of 3H in both Ve and Vp preparations pre-loaded with 3H-NA. Phenylephrine, prazosin, isoprenaline, propranolol, carbachol and scopolamine had minor or no effects on the 3H release. Radioligand receptor binding experiments using 3H-prazosin and 3H-rauwolscine as ligands revealed similar densities of alpha 1- and alpha 2-adrenoreceptors in the human vas deferens. There seemed to be no differences in their distribution between the epididymal, middle and prostatic part of the organ. It is concluded that the neurotransmission in the human vas deferens is noradrenergic and mediated via alpha 1-adrenoreceptors. The prazosin and tetrodotoxin resistant part of the electrically induced contraction in Vp preparations may be caused by direct smooth muscle stimulation.
对人离体输精管附睾段(Ve)和前列腺段(Vp)的环形标本进行电场刺激,可产生频率依赖性和外观相似的收缩。河豚毒素(10⁻⁶M)可消除Ve标本的收缩,但不能消除Vp标本的收缩。去甲肾上腺素(NA)、去氧肾上腺素和甲氧明可在Ve和Vp标本中诱导重复性、阶段性收缩,并增加电诱导反应的幅度,但可乐定无此作用。可乐定浓度依赖性地降低Ve标本中的电诱导收缩,但对Vp标本无显著影响。酚妥拉明和哌唑嗪可消除Ve标本中的电诱导收缩,但不能消除Vp标本中的收缩。在Ve环中,萝芙辛可增强收缩;在Vp标本中未观察到这种作用。异丙肾上腺素、普萘洛尔、乙酰胆碱和卡巴胆碱对Ve或Vp标本均无作用。东莨菪碱和阿托品可降低电诱导反应。可乐定可降低,萝芙辛可增加预先加载3H-NA的Ve和Vp标本中3H的电诱导释放。去氧肾上腺素、哌唑嗪、异丙肾上腺素、普萘洛尔、卡巴胆碱和东莨菪碱对3H释放的影响较小或无影响。以3H-哌唑嗪和3H-萝芙辛为配体的放射性配体受体结合实验表明,人输精管中α1-和α2-肾上腺素能受体密度相似。在该器官的附睾段、中段和前列腺段之间,其分布似乎没有差异。结论是,人输精管中的神经传递是去甲肾上腺素能的,并通过α1-肾上腺素能受体介导。Vp标本中电诱导收缩对哌唑嗪和河豚毒素耐药的部分可能是由直接平滑肌刺激引起的。