胰岛素瘤细胞中ATP敏感性钾通道的调节：生长抑素和蛋白激酶C的激活以及环磷酸腺苷的作用
Regulation of ATP-sensitive K+ channels in insulinoma cells: activation by somatostatin and protein kinase C and the role of cAMP.
作者信息
de Weille J R, Schmid-Antomarchi H, Fosset M, Lazdunski M
机构信息
Centre de Biochimie du Centre National de la Recherche Scientifique, Nice, France.
出版信息
Proc Natl Acad Sci U S A. 1989 Apr;86(8):2971-5. doi: 10.1073/pnas.86.8.2971.
The actions of somatostatin and of the phorbol ester 4 beta-phorbol 12-myristate 13-acetate (PMA) were studied in rat insulinoma (RINm5F) cells by electrophysiological and 86Rb+ flux techniques. Both PMA and somatostatin hyperpolarize insulinoma cells by activating ATP-sensitive K+ channels. The presence of intracellular GTP is required for the somatostatin effects. PMA- and somatostatin-induced hyperpolarization and channel activity are inhibited by the sulfonylurea glibenclamide. Glibenclamide-sensitive 86Rb+ efflux from insulinoma cells is stimulated by somatostatin in a dose-dependent manner (half maximal effect at 0.7 nM) and abolished by pertussis toxin pretreatment. Mutual roles of a GTP-binding protein, of protein kinase C, and of cAMP in the regulation of ATP-sensitive K+ channels are discussed.
采用电生理学和⁸⁶Rb⁺通量技术，在大鼠胰岛素瘤（RINm5F）细胞中研究了生长抑素和佛波酯4β-佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）的作用。PMA和生长抑素均通过激活ATP敏感性钾通道使胰岛素瘤细胞超极化。生长抑素发挥作用需要细胞内GTP的存在。磺酰脲类药物格列本脲可抑制PMA和生长抑素诱导的超极化及通道活性。生长抑素以剂量依赖性方式刺激胰岛素瘤细胞中格列本脲敏感的⁸⁶Rb⁺外流（半数最大效应浓度为0.7 nM），百日咳毒素预处理可消除该作用。文中讨论了GTP结合蛋白、蛋白激酶C和cAMP在ATP敏感性钾通道调节中的相互作用。
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