β-肾上腺素能受体介导延迟整流钾电流增加的机制
Mechanisms of beta-adrenoceptor mediated increase in delayed rectifier potassium current.
作者信息
Iijima T, Taira N
机构信息
Department of Pharmacology, Tohoku University School of Medicine, Sendai, Japan.
出版信息
Tohoku J Exp Med. 1989 Dec;159(4):277-81. doi: 10.1620/tjem.159.277.
Experiments were carried out in single ventricular cells of the guinea-pig heart. Isoproterenol, forskolin, intracellularly applied cyclic AMP and 3-isobutyl-1-methylxanthine increased the delayed rectifier potassium current (IK). The effect of isoproterenol was abolished by intracellularly applied guanosine 5'-O-(3-thio-triphosphate). These results indicate that isoproterenol stimulates beta-adrenoceptors to activate adenylate cyclase by mediation through the stimulatory GTP-binding protein, and causes an increase in intracellular cyclic AMP levels. Then IK is probably increased by phosphorylation of the IK-channel protein by cyclic AMP-dependent protein kinase.
实验在豚鼠心脏的单个心室肌细胞中进行。异丙肾上腺素、福斯高林、细胞内应用的环磷酸腺苷（cAMP）和3 - 异丁基 - 1 - 甲基黄嘌呤增加了延迟整流钾电流（IK）。细胞内应用鸟苷5'-O-（3 - 硫代三磷酸）可消除异丙肾上腺素的作用。这些结果表明，异丙肾上腺素通过刺激型GTP结合蛋白介导刺激β - 肾上腺素能受体激活腺苷酸环化酶，导致细胞内环磷酸腺苷水平升高。然后，IK可能通过环磷酸腺苷依赖性蛋白激酶对IK通道蛋白的磷酸化而增加。
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