U50,488H对正常及缺氧心肌细胞钾电流的作用  

Effects of U50,488H on potassium current in ventricular myocytes of normal and hypoxic rats

作　　者：毕辉[1] 郭海涛[1] 仝黎[1] 吕顺艳[1] 王跃民[1] 裴建明[1] 

机构地区：[1]第四军医大学生理学教研室,陕西西安710032

出　　处：《中国现代医学杂志》2007年第15期1814-1817,共4页China Journal of Modern Medicine

基　　金：国家自然科学基金面上项目(30370580);全军医药卫生科研基金军队"十一五"计划面上项目(编号:06MA203)

摘　　要：目的观察U50,488H(κ阿片受体选择性激动剂)对正常及缺氧心肌细胞钾电流的影响。方法采用全细胞膜片钳技术,记录了急性分离的正常及缺氧大鼠心室肌细胞的钾电流。结果U50,488H(1～500μmol/L)可以剂量依赖性地抑制正常心肌细胞的钾电流,该作用可被κ阿片受体特异性阻断剂Nor-BNI(100μmol/L)所阻断。而细胞缺氧后,钾电流虽有所下降,但与正常对照差异无显著性。U50,488H(1～500μmol/L)可以剂量依赖性地抑制低氧心肌细胞的钾电流,并且U50,488H对心肌细胞钾通道电流的抑制作用不受缺氧的影响。结论心脏阿片受体参与了对心脏钾离子通道功能的调节,这可能是阿片类物质抗心律失常的原因之一。[Objective] To investigate the effects of U50, 488H, a selective κ-opioid receptor agonist, on potassium currents （It,） in the normal and hypoxic rat ventricular myocytes. [Methods] Whole-cell patch clamp technique was used to examine the Ik of normal and hypoxia isolated ventricular myocytes. [Results] The IK was inhibited by U50, 488H （1～500 μmol/L） in a dose-dependent manner in normal and hypoxic rat ventricular myocytes. And the effect of U50, 488H was blocked by Nor-BNI （100 μmol/L）, a selective K-opioid receptor antagonist. U50, 488H did not show significantly different effects in normal and hypoxia myocytes. [Conclusion] The results indicate that κ-opioid receptor participates in the regulation of potassium channels in the ventricular myoeytes, which maybe the important reason for the anti-arrhythmic effect of κ-opioids.

关 键 词：Κ阿片受体 U50 488H 钾离子通道 心肌细胞 缺氧 

分 类 号：R331.3[医药卫生—人体生理学]