Diener M, Knobloch S F, Rummel W
Institut für Pharmakologie und Toxikologie, Universität des Saarlandes, Homburg/Saar, F.R.G.
Eur J Pharmacol. 1988 Aug 2;152(3):217-25. doi: 10.1016/0014-2999(88)90716-9.
The action of loperamide on the ion secretion evoked in rat colon descendens by electric field stimulation of enteric neurons, on the Ca2+-dependent secretion due to carbachol, and on the cAMP-mediated secretion elicited by forskolin was studied. Loperamide blocked all three types of secretion, but about 10 times higher concentrations of the drug were necessary to block the secretion caused by forskolin than to block the secretion mediated neuronally or by Ca2+. All the effects of loperamide were mimicked by trifluoperazine, a calmodulin antagonist. Neither morphine nor the Ca2+ channel blocker, verapamil, mimicked the effects of loperamide on ion transport. Therefore it seems reasonable to conclude that the antisecretory action of loperamide in the rat colon is caused by a block of the calmodulin system.
研究了洛哌丁胺对肠神经元电场刺激诱发的大鼠降结肠离子分泌、对卡巴胆碱引起的钙依赖性分泌以及对福斯可林引发的环磷酸腺苷(cAMP)介导的分泌的作用。洛哌丁胺可阻断所有这三种类型的分泌,但阻断福斯可林引起的分泌所需药物浓度比阻断神经介导或钙介导的分泌高出约10倍。钙调蛋白拮抗剂三氟拉嗪可模拟洛哌丁胺的所有作用。吗啡和钙通道阻滞剂维拉帕米均不能模拟洛哌丁胺对离子转运的作用。因此,似乎有理由得出结论,洛哌丁胺在大鼠结肠中的抗分泌作用是由钙调蛋白系统的阻断引起的。