首页> 美国卫生研究院文献>British Journal of Pharmacology and Chemotherapy >The differential contribution of endogenous prostaglandins to the release of acetylcholine from the myenteric plexus of the guinea-pig ileum.
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The differential contribution of endogenous prostaglandins to the release of acetylcholine from the myenteric plexus of the guinea-pig ileum.

机译:内源性前列腺素对豚鼠回肠肌层神经丛释放乙酰胆碱的贡献不同。

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摘要

1. 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.
机译:1.前列腺素E(PGE)对于维持豚鼠回肠的肌间神经丛对尼古丁的敏感性可能是必不可少的。现在已经通过测量从豚鼠回肠的肌间神经丛释放的乙酰胆碱(ACh)的量来研究前列腺素对不同刺激引起的神经活动的贡献。 2. 2.8 microM吲哚美辛(Ind)将响应二甲基苯基哌嗪鎓(DMPP)或P物质释放的ACh量降低至对照的40%,而5-羟基色胺(5-HT)诱导的ACh释放未降低受到影响。 14.3 nM PGE2克服了Ind的抑制作用。 3. Mepacrine 5 microM,一种磷脂酶A2的抑制剂,与Ind一样,抑制了DMPP和P物质对ACh的释放,花生四烯酸(10 microM)克服了Mepacrine的这些抑制作用,但花生四烯酸却没有5-羟色胺或电场刺激(EFS)引起的乙酰胆碱的释放也被美帕克林抑制到对照的约60%,但花生四烯酸(10 microM)在不存在或存在下均可克服这些抑制作用4.结果表明,内源性前列腺素和花生四烯酸有助于维持DMPP和P物质对肌层神经丛的兴奋性。相反,花生四烯酸可调节5-HT和EFS诱导的ACh释放。酸而不是前列腺素。

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