Sawynok J, Jhamandas K
Can J Physiol Pharmacol. 1977 Aug;55(4):909-16. doi: 10.1139/y77-121.
Atropine (10(-8)-10(-6) M) produced a dose-related increase in the release of ACh from the electrically stimulated longitudinal muscle-myenteric plexus preparation. This increase in release was frequency dependent, being greater at low frequencies of stimulation where the pulse release of ACh was greater than at high frequencies. The muscarinic agonist oxotremorine (up to 100 micrometer) did not inhibit ACh release although 100 micrometer oxotremorine did antagonize the ability of atropine to increase release. The effect of chronic exposure to morphine, both in vivo and in vitro, on the reactivity of muscarinic receptors mediating this increase was examined. Neither the control rate of ACh release nor the dose-response curve for atropine were altered by (a) an 8-day morphine injection schedule, and (b) exposure of the tissue to morphine in the bath for 90 min. The results of this study support the existence of a muscarinic feedback mechanism which controls ACh release from the myenteric plexus. Chronic exposure to morphine does not produce specific changes in the muscarinic receptor mediating this inhibition.
阿托品(10⁻⁸ - 10⁻⁶ M)使电刺激的纵行肌-肠肌丛标本中乙酰胆碱(ACh)的释放呈剂量依赖性增加。这种释放增加与频率有关,在低频刺激时更大,此时ACh的脉冲释放量高于高频刺激时。毒蕈碱激动剂氧化震颤素(高达100微摩尔)并不抑制ACh释放,尽管100微摩尔氧化震颤素确实拮抗了阿托品增加释放的能力。研究了体内和体外长期暴露于吗啡对介导这种增加的毒蕈碱受体反应性的影响。(a)8天的吗啡注射方案以及(b)将组织在浴中暴露于吗啡90分钟,均未改变ACh的对照释放速率或阿托品的剂量反应曲线。本研究结果支持存在一种控制肠肌丛ACh释放的毒蕈碱反馈机制。长期暴露于吗啡不会在介导这种抑制作用的毒蕈碱受体上产生特异性变化。