Das M, Ganguly D K
Eur J Pharmacol. 1984 Apr 13;100(1):41-6. doi: 10.1016/0014-2999(84)90313-3.
The effect of prostaglandin E2 (PGE2) on the acetylcholine (ACh) release evoked from rat phrenic nerve terminals and from Auerbach's plexus of the guinea-pig ileum was investigated. PGE2 enhanced the evoked release of ACh from phrenic nerve terminals and from Auerbach's plexus in a concentration-dependent manner. Preincubation with 7-oxa-13-prostynoic acid, the PGE receptor blocker, and indomethacin inhibited the PGE2-induced increase of evoked release of ACh while atropine failed to do so. Whereas a single administration of either 7-oxa-13-prostynoic acid or indomethacin significantly inhibited the control evoked release of ACh from the Auerbach's plexus, they failed to alter the control evoked release of ACh from the phrenic nerve terminals. The study indicates that the PGE2-induced increase in release of ACh from cholinergic nerve terminals is accomplished through activation of prostaglandin receptors and that PGE2 may play a physiological role in ACh liberation from the cholinergic autonomic nerve terminals but not from motor nerve terminals.
研究了前列腺素E2(PGE2)对大鼠膈神经末梢以及豚鼠回肠奥尔巴赫神经丛诱发的乙酰胆碱(ACh)释放的影响。PGE2以浓度依赖性方式增强了膈神经末梢和奥尔巴赫神经丛诱发的ACh释放。用PGE受体阻滞剂7-氧杂-13-前列腺炔酸和吲哚美辛预孵育可抑制PGE2诱导的诱发ACh释放增加,而阿托品则无此作用。虽然单次给予7-氧杂-13-前列腺炔酸或吲哚美辛可显著抑制奥尔巴赫神经丛的对照诱发ACh释放,但它们未能改变膈神经末梢的对照诱发ACh释放。该研究表明,PGE2诱导的胆碱能神经末梢ACh释放增加是通过前列腺素受体激活实现的,并且PGE2可能在胆碱能自主神经末梢而非运动神经末梢的ACh释放中发挥生理作用。