Gylfe E
Department of Medical Cell Biology, Uppsala University, Sweden.
Naunyn Schmiedebergs Arch Pharmacol. 1992 Feb;345(2):235-7. doi: 10.1007/BF00165742.
The effect of BAY K 8644 on the cytoplasmic Ca2+ concentration ([Ca2+]i) was studied in pancreatic beta-cells hyperpolarized by the K+ channel-activating agent diazoxide. After 50-60 min preexposure to 0-20 mM glucose in the presence of 400 microM diazoxide [Ca2+]i was close to the level in unstimulated beta-cells. The addition of 5 microM BAY K 8644 then triggered a rise of [Ca2+]i dependent on Ca2+ influx. The magnitude of the BAY K 8644 effect increased with the glucose concentration and was almost 10-fold higher in 20 mM than in the absence of the sugar. It is concluded that glucose can modulate Ca2+ entry through the voltage-dependent channels by a mechanism additional to depolarization. This action may help to explain why previous exposure to the sugar results in an augmented insulin response to a second challenge.
在通过钾通道激活剂二氮嗪超极化的胰腺β细胞中，研究了BAY K 8644对细胞质钙离子浓度（[Ca2+]i）的影响。在存在400微摩尔二氮嗪的情况下，预先暴露于0 - 20毫摩尔葡萄糖50 - 60分钟后，[Ca2+]i接近未受刺激的β细胞中的水平。然后添加5微摩尔BAY K 8644会引发依赖于钙离子内流的[Ca2+]i升高。BAY K 8644效应的幅度随葡萄糖浓度增加，在20毫摩尔葡萄糖时比无糖时高近10倍。结论是，葡萄糖可通过除去极化之外的机制调节通过电压依赖性通道的钙离子内流。这一作用可能有助于解释为什么先前暴露于该糖类会导致对第二次刺激的胰岛素反应增强。
