Wang X B, Osugi T, Uchida S
Department of Pharmacology, Osaka University School of Medicine, Japan.
Biochem Biophys Res Commun. 1993 Jun 15;193(2):483-9. doi: 10.1006/bbrc.1993.1649.
Receptor-mediated changes in intracellular Ca2+ in ileal longitudinal smooth muscles of guinea pig were studied. Stimulation of muscarinic receptors by carbachol induced both Ca(2+)-influx through plasma membranes and Ca(2+)-release from intracellular stores. Pretreatment of the muscle with an inhibitor of phospholipase A2 abolished the Ca2+ influx but not the Ca(2+)-release, whereas an inhibitor of phospholipase C showed opposite effects. The inhibitors of cyclooxygenase and lipoxygenase enhanced the muscarinic receptor-induced Ca(2+)-influx. Addition of arachidonic acid mimic the receptor-induced Ca(2+)-influx. Treatment of muscles with pertussis toxin abolished the receptor-induced release of arachidonic acid as well as Ca(2+)-influx, but was less effective on the IP3 formation and the Ca(2+)-release. Taken together, our results suggest that phospholipase A2 but not phospholipase C pathway is involved in the muscarinic receptor-induced Ca(2+)-influx in ileal smooth muscle.
研究了豚鼠回肠纵行平滑肌中受体介导的细胞内钙离子变化。卡巴胆碱刺激毒蕈碱受体可诱导钙离子通过质膜内流以及从细胞内储存库释放。用磷脂酶A2抑制剂预处理肌肉可消除钙离子内流，但不能消除钙离子释放，而磷脂酶C抑制剂则表现出相反的效果。环氧化酶和脂氧合酶抑制剂增强了毒蕈碱受体诱导的钙离子内流。添加花生四烯酸可模拟受体诱导的钙离子内流。用百日咳毒素处理肌肉可消除受体诱导的花生四烯酸释放以及钙离子内流，但对肌醇三磷酸形成和钙离子释放的作用较小。综上所述，我们的结果表明，磷脂酶A2而非磷脂酶C途径参与了毒蕈碱受体诱导的回肠平滑肌钙离子内流。
