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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
OBJECTIVE: To investigate the characteristics of α1B adrenergic receptor subtypes in HEK293 cells that cause outward K + currents and Ca2 + influx. Methods: Cytosolic Ca2 + concentration was measured by single cell recording of K + channels and Fura2 fluorescence. Results: Epinephrine or phenylephrine induces an outward K + current with a conductance of 160 pS. The current can be inhibited by 50μmol·L-1 CEC, 5mmol·L-1 EGTA or 2mmol·L-1 tetraethylammonium (TEA). Nifedipine did not alter Ca2 + influx induced by this current and α1B subtype; the latter could be inhibited by 1 mmol·L-1 LaCl3. Conclusion: Activation of the α1B receptor subtype transfected on HEK293 cells causes Ca2 + influx through the nifedipine-insensitive Ca2 + channels and follows the generation of an outward K + current