Lee C M
Br J Pharmacol. 1985 Nov;86(3):671-6. doi: 10.1111/j.1476-5381.1985.tb08944.x.
Cholinoceptor agonists (arecoline congruent to carbachol greater than acetylcholine greater than pilocarpine) potentiated contractions to field stimulation of rat vas deferens via the activation of an atropine-sensitive muscarinic receptor. The potentiating effect of carbachol was dependent on the level of calcium in the medium, being more potent at higher calcium concentrations. The potentiating effect of carbachol was more pronounced in the epididymal than in the prostatic segment but was not attenuated by prazosin, an alpha 1-adrenoceptor antagonist. Carbachol did not significantly modify the direct contractile effects of noradrenaline nor alter the field-stimulation-evoked release of noradrenaline from the epididymal vas deferens. It is concluded that the potentiating effect of cholinoceptor agonists on the contractions to field stimulation in the rat vas deferens was not a result of an enhancement of adrenergic neurotransmission.
胆碱受体激动剂(槟榔碱等同于卡巴胆碱大于乙酰胆碱大于毛果芸香碱)通过激活对阿托品敏感的毒蕈碱受体,增强大鼠输精管对场刺激的收缩作用。卡巴胆碱的增强作用取决于培养基中的钙水平,在较高钙浓度下作用更强。卡巴胆碱在附睾段的增强作用比前列腺段更明显,但不被α1-肾上腺素能受体拮抗剂哌唑嗪减弱。卡巴胆碱不会显著改变去甲肾上腺素的直接收缩作用,也不会改变附睾输精管场刺激诱发的去甲肾上腺素释放。结论是,胆碱受体激动剂对大鼠输精管场刺激收缩的增强作用不是肾上腺素能神经传递增强的结果。