G蛋白对血管紧张素Ⅱ抑制ECV304钙激活钾通道的调节效应  

G-protein Modulates the Inhibition of Angiotensin Ⅱ on BK_(Ca) in ECV304

作　　者：林琳[1] 郑永芳[1] 屈金河[1] 鲍光宏[1] 

机构地区：[1]中国医学科学院中国协和医科大学基础医学研究所生理室,北京100005

出　　处：《中国医学科学院学报》2000年第4期336-339,共4页Acta Academiae Medicinae Sinicae

基　　金：国家自然科学基金重点项目!( 3 973 0 2 2 0 )&&

摘　　要：目的　探讨血管紧张素 (A )对人脐静脉内皮细胞株 ECV 30 4大电导钙激活钾通道 (BKCa)的影响及 G蛋白在此过程中的作用。方法　用细胞贴附式膜片箝技术记录 BKCa的活动电流。结果　 10 - 7mol/ L A 可抑制 ECV30 4细胞膜上 BKCa的活动 ,表现为电流幅值下降 ,开放概率减小 ,通道开放时间缩短 ,关闭时间延长 ;G蛋白稳定激动剂 GTPγS可对抗 A 的抑制效应 ,G蛋白稳定抑制剂 GDPβS则增强 A 的抑制效应。结论　 A 可明显减弱 ECV30 4细胞膜上 BKCa的活动 ,使膜向着去极化方向发展 ,从而改变膜的稳定性 ,导致内皮细胞功能障碍。 G蛋白在此过程中起调节作用。Objective To investigate the effect of angiotensin Ⅱ(AⅡ) on maxi conductance calcium activated potassium channel(BK Ca ) activity in ECV304 cell membrane,and the possible involvement of G protein. Methods Cell attached configuration of patch clamp technique was employed to record the current of BK Ca in ECV304. Results 10 -7 mol/L angiotensin Ⅱ inhibited the BK Ca activity. Current amplitude and open probability were decreased, open time was shortened and close time was increased. G protein activation could eliminate the inhibition of AⅡ. Conclusions AⅡ significantly decreased the activity of BK Ca in ECV304,which might depolarize the membrane,and the stability of membrane might change. Thus endothelial cell dysfunction might be induced. G protein activation was involved in the regulation of the above AⅡ inhibition process.

关 键 词：钙激活钾通道 血管紧张素Ⅱ 血管内皮细胞 G蛋白 

分 类 号：R322.123[医药卫生—人体解剖和组织胚胎学]