Yagasaki O, Funaki H, Yanagiya I
Eur J Pharmacol. 1984 Aug 3;103(1-2):1-8. doi: 10.1016/0014-2999(84)90182-1.
The role of endogenous prostaglandins (PGs) in the nicotine-induced contraction and release of ACh was investigated in the isolated guinea-pig ileum. A low concentration of indomethacin (IND 2.8 microM) inhibited the contraction and ACh release induced by nicotine. These inhibitory effects of IND were reversed by PGE2 at concentrations which are thought to be released spontaneously. SC-19220, a PG receptors antagonist, also inhibited the contraction and ACh release induced by nicotine. Unlike the nicotine-induced release of ACh, the potassium-induced release of ACh was unaffected by IND and SC-19220. IND was as potent in inhibiting the responses to cholinergic nerve stimulation by nicotine after treatment of the preparations with antiadrenergic agents. It is concluded that the inhibitory effect of IND does not depend on the functional integrity of adrenergic neurons and that endogenous PGs contribute directly to the modulation of myenteric plexus excitability by nicotine.
在离体豚鼠回肠中研究了内源性前列腺素（PGs）在尼古丁诱导的收缩和乙酰胆碱（ACh）释放中的作用。低浓度的吲哚美辛（IND 2.8微摩尔）抑制尼古丁诱导的收缩和ACh释放。吲哚美辛的这些抑制作用被认为是自发释放的浓度的前列腺素E2（PGE2）所逆转。PG受体拮抗剂SC-19220也抑制尼古丁诱导的收缩和ACh释放。与尼古丁诱导的ACh释放不同，钾诱导的ACh释放不受吲哚美辛和SC-19220的影响。在用抗肾上腺素能药物处理标本后，吲哚美辛在抑制尼古丁对胆碱能神经刺激的反应方面同样有效。得出的结论是，吲哚美辛的抑制作用不依赖于肾上腺素能神经元的功能完整性，并且内源性PGs直接参与尼古丁对肠肌间神经丛兴奋性的调节。
