节点文献

HEK-293细胞α1B-肾上腺素受体引起的Ca2+依赖性K+电流和Ca2+内流(英文)

Study in the Ca2+ Dependent K+ Current and Ca2+ Entry Induced by Activation of α1B Adrenoceptor Subtype in HEK 293 Cell

  • 推荐 CAJ下载
  • PDF下载
  • 不支持迅雷等下载工具,请取消加速工具后下载。

【作者】 关永源陶亮贺华韩启德张幼怡孙家钧

【Author】 Guan Yongyuan 1 Tao Liang 1 He Hua 1 Han Qide 2 Zhang Youyi 2 Sun Jiajun 1 ( 1 Department of Pharmacology, Sun Yat sen University of Medical Sciences, Guangzhou, 510089 2 Institute of Vascular Medicine, Beijing Medical University, Beijing,100083)$$$$

【机构】 中山医科大学药理教研室北京医科大学血管医学研究所!北京100083

【摘要】 目的:研究HEK293细胞上α1B肾上腺素受体亚型引起向外K+电流和Ca2+内流的特性。方法:细胞贴附式单通道记录K+通道和Fura2荧光测定胞浆游离Ca2+浓度。结果:肾上腺素或苯肾上腺素可引发一电导为160pS的外向K+电流。该电流可被50μmol·L-1氯乙醛可乐定(CEC),5mmol·L-1依他酸(EGTA)或2mmol·L-1四乙铵(TEA)抑制。硝苯吡啶(nifedipine)不改变该电流及α1B亚型引起的Ca2+内流;后者可被1mmol·L-1LaCl3抑制。结论:激活转染在HEK293细胞上的α1B受体亚型可引起通过硝苯吡啶不敏感Ca2+通道的Ca2+内流,并跟随产生-外向K+电流

【Abstract】 Objective: To study the characterization of the outward K + current and Ca 2+ entry induced by activation of α 1B adrenoceptor subtype at the HEK 293 cells. Methods: The single K + current was recorded from the cell attached configuration. The cytoplasmic Ca 2+ was measured by fura 2 probe. Results: adrenaline evoked an outward K + current with a conductance of 160 pS. The current was markedly inhibited by 50 μmol·L -1 chloroethylclonidine, 5 mmol·L -1 EGTA or 2 mmol·L -1 TEA. Nifedipine did not change this current and adrenaline induced Ca 2+ entry wihich was inhibited by 1 mmol·L -1 LaCl 3. Conclusion: Activation of α 1B subtype receptor at HEK 293 cells evokes Ca 2+ entry through the nifedipine resistant Ca 2+ channel, followed by an outward K~+ current.

  • 【文献出处】 中山医科大学学报 ,Academic Journal of Sun Yat-sen University of Medical Sciences , 编辑部邮箱 ,1999年04期
  • 【分类号】R363
  • 【下载频次】91
节点文献中: 

本文链接的文献网络图示:

本文的引文网络