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G蛋白在亮啡肽诱导心肌细胞内钙释放中的作用

魏振宇, 谈世进, 唐二虎, 潘敬运, 詹澄扬

遵义医学院生理教研室. 贵州, 遵义 563003；中山医科大学生理学教研室. 广东, 广州 510089

摘要

分离的SD大鼠心室肌细胞, 以Fura-2AM荧光指示剂负载, 检测心肌细胞内游离钙浓度([Ca~(2+)]_(i))变化。结果表明, 亮啡肽(LEK 60#mu#mol/L)能升高[Ca~(2+)]; 移去细胞外液钙此效应仍能出现, 用caffeine(5 mmol/L)耗竭细胞内钙池的钙, 该效应消失, 钠洛酮(100 #mu#mol/L)、百日咳毒素(200ng/L)处理8-10h及procaine(2mmol/L)都能阻断该效应。以上结果表明: 亮啡肽诱导[Ca~(2+)_(i)升高是通过#delta#受体 与百日咳毒素敏感的G蛋白耦联并诱导心肌细胞内钙释放所引起。图4参14

关键词： 心肌细胞; 亮啡肽; δ受体; G蛋白; 游离钙

The role of G protein in Leu-enkephalin induced Ca~(2+)release from intracellular pool in myocytes

Wei Zhenyu, Tan Shijin, Tang Erhu, Pan Jingyun, Zhan Chengyang

Department of Physiology, Zunyi Medical College. Zunyi 563003, Guizhou；China

Abstract

The mechanism underlying Leu--enkephalin (LEK) induced increase of the intracellular concentration of free calcium ([ca~(2+)]i) in rat ventricular myocytes was investigated by using fura--2 AM as a calcium indicator. The results were as follows: KEK (60 #mu#mol/L) elevated [Ca~(2+)]i in ventricular myocytes to matter whether extracellular calcium was removed or not. However, the effect was no longer observed when the calcium in the intracellular pool was depleted by caffeine (5 mmol/L). The LEK effect could also be blocked by naloxone (100 #mu#mol/L), pretreatment of the cells with PTX (200 ng/L) 8--10 h or procain (2 mmol/L). The results suggest that the LEK effect is mediated by coupling of G--protein with #delta#--receptor that induced Ca~(2+)release from the intracellular pool in myocytes.

Key words: Myocyte;Leu-enkephalin;#delta#-receptor;G-protein;Free calcium

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引用本文：

魏振宇, 谈世进, 唐二虎, 潘敬运, 詹澄扬. G蛋白在亮啡肽诱导心肌细胞内钙释放中的作用[J]. 生理学报 1995; 47 (2): .

Wei Zhenyu, Tan Shijin, Tang Erhu, Pan Jingyun, Zhan Chengyang. The role of G protein in Leu-enkephalin induced Ca~(2+)release from intracellular pool in myocytes. Acta Physiol Sin 1995; 47 (2): (in Chinese with English abstract).