Fosset M, Schmid-Antomarchi H, de Weille J R, Lazdunski M
Centre de Biochimie, Centre National de la Recherche Scientifique, Nice, France.
FEBS Lett. 1988 Dec 19;242(1):94-6. doi: 10.1016/0014-5793(88)80992-x.
Somatostatin, an hyperglycemia-inducing hormone, was studied in rat insulinoma (RINm5F) cells using 86Rb+ efflux techniques. 86Rb+ efflux is stimulated by somatostatin in a dose-dependent manner. The half-maximum value of activation is 0.7 nM. Somatostatin-induced 86Rb+ efflux is abolished by the hypoglycemia-inducing sulfonylurea, glibenclamide, a known blocker of ATP-regulated K+ channels. Somatostatin activation is prevented by pretreatment of insulinoma cells with pertussis toxin. 86Rb+ efflux studies show that somatostatin activates an ATP-dependent K+ channel.
生长抑素是一种可诱导高血糖的激素，本研究利用⁸⁶Rb⁺外流技术在大鼠胰岛素瘤（RINm5F）细胞中对其进行了研究。生长抑素以剂量依赖的方式刺激⁸⁶Rb⁺外流。激活的半数最大值为0.7 nM。可诱导低血糖的磺脲类药物格列本脲（一种已知的ATP调节钾通道阻滞剂）可消除生长抑素诱导的⁸⁶Rb⁺外流。用百日咳毒素预处理胰岛素瘤细胞可阻止生长抑素的激活。⁸⁶Rb⁺外流研究表明，生长抑素激活了一种ATP依赖的钾通道。
