内源性前列腺素对豚鼠回肠肌间神经丛乙酰胆碱释放的不同贡献。

The differential contribution of endogenous prostaglandins to the release of acetylcholine from the myenteric plexus of the guinea-pig ileum.

Takeuchi T, Okuda M, Yagasaki O

Department of Veterinary Pharmacology, Faculty of Agriculture, University of Osaka Prefecture, Sakai, Japan.

Br J Pharmacol. 1991 Feb;102(2):381-5. doi: 10.1111/j.1476-5381.1991.tb12182.x.

Abstract

Prostaglandin E (PGE) may be essential for maintaining the sensitivity of the myenteric plexus of guinea-pig ileum to nicotine. The contributions of prostaglandins to nervous activity evoked by different stimuli have now been investigated by measuring the amount of acetylcholine (ACh) released from the myenteric plexus of the guinea-pig ileum. 2. The amount of ACh released in response to dimethylphenylpiperazinium (DMPP) or substance P was depressed to about 40% of control by 2.8 microM indomethacin (Ind), whereas the release of ACh induced by 5-hydroxytryptamine (5-HT) was not affected. The inhibitory effects of Ind were overcome by 14.3 nM PGE2. 3. Mepacrine 5 microM, an inhibitor of phospholipase A2, depressed the release of ACh in response to DMPP and substance P to the same extent as Ind. These inhibitory effects of mepacrine were overcome by arachidonic acid (10 microM), but not by arachidonic acid plus Ind. The release of ACh evoked by 5-HT or electrical field stimulation (EFS) was also inhibited to about 60% of control by mepacrine but these inhibitions were overcome by arachidonic acid (10 microM) either in the absence or the presence of Ind. 4. The results suggest that endogenous prostaglandins and arachidonic acid contribute to the maintenance of the excitability of the myenteric plexus by DMPP and substance P. By contrast, the release of ACh induced by 5-HT and EFS may be regulated by arachidonic acid and not by prostaglandins.

摘要

前列腺素E（PGE）对于维持豚鼠回肠肌间神经丛对尼古丁的敏感性可能至关重要。现在，通过测量豚鼠回肠肌间神经丛释放的乙酰胆碱（ACh）量，研究了前列腺素对不同刺激诱发的神经活动的作用。2. 2.8微摩尔吲哚美辛（Ind）使对二甲基苯基哌嗪（DMPP）或P物质产生反应而释放的ACh量降低至对照的约40%，而5-羟色胺（5-HT）诱导的ACh释放不受影响。14.3纳摩尔前列腺素E2可克服吲哚美辛的抑制作用。3. 5微摩尔氯喹，一种磷脂酶A2抑制剂，使对DMPP和P物质产生反应而释放的ACh量降低到与吲哚美辛相同的程度。氯喹的这些抑制作用可被花生四烯酸（10微摩尔）克服，但不能被花生四烯酸加吲哚美辛克服。5-HT或电场刺激（EFS）诱发的ACh释放也被氯喹抑制至对照的约60%，但这些抑制作用在不存在或存在吲哚美辛的情况下均可被花生四烯酸（10微摩尔）克服。4. 结果表明，内源性前列腺素和花生四烯酸有助于维持肌间神经丛对DMPP和P物质的兴奋性。相比之下，5-HT和EFS诱导的ACh释放可能受花生四烯酸调节，而不受前列腺素调节。