Yagasaki O, Takai M, Yanagiya I
J Pharm Pharmacol. 1981 Aug;33(8):521-5. doi: 10.1111/j.2042-7158.1981.tb13851.x.
Release of acetylcholine (ACh) by prostaglandin E1 from the nerve terminals of the guinea-pig longitudinal muscle strip was studied in order to reveal the effect of PGE1 on myenteric plexus activity. The ACh released was collected in the presence of physostigmine (2.1 microgram ml-1) and choline (0.1 microgram ml-1) at 38 degrees C. Five to 100 ng ml-1 PGE1 enhanced the release dose-dependently. The effect was maintained during the presence of PGE1 in the organ bath, while rapid tachyphylaxis was observed with the ACh-releasing action of nicotine. Tetrodotoxin or morphine almost completely inhibited the effect of PGE1 on ACh release. Hexamethonium, in a concentration which completely blocked the effect of nicotine, partially inhibited the effect of PGE1. In the late phase of nicotine action, the tissue was still sensitive to PGE1 despite the continued exposure to nicotine. These data suggest the presence in the myenteric plexus of PG receptors which can increase ACh release.
为了揭示前列腺素E1(PGE1)对肠肌间神经丛活性的影响,研究了PGE1从豚鼠纵行肌条神经末梢释放乙酰胆碱(ACh)的情况。在38℃下,于毒扁豆碱(2.1微克/毫升)和胆碱(0.1微克/毫升)存在的条件下收集释放的ACh。5至100纳克/毫升的PGE1可剂量依赖性地增强释放。在器官浴中存在PGE1期间该效应持续存在,而尼古丁的ACh释放作用则出现快速耐受性。河豚毒素或吗啡几乎完全抑制PGE1对ACh释放的作用。六甲铵在完全阻断尼古丁作用的浓度下,部分抑制PGE1的作用。在尼古丁作用的后期,尽管持续暴露于尼古丁,组织对PGE1仍敏感。这些数据表明肠肌间神经丛中存在可增加ACh释放的PG受体。