HEK-293细胞α_(1B)-肾上腺素受体引起的Ca^(2+)依赖性K^+电流和Ca^(2+)内流(英文)

Study in the Ca^(2+) Dependent K^+ Current and Ca^(2+) Entry Induced by Activation of α_(1B) Adrenoceptor Subtype in HEK 293 Cell

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。

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.