Takano M, Ashcroft F M
University Laboratory of Physiology, Oxford, UK.
Pflugers Arch. 1994 Sep;428(2):194-6. doi: 10.1007/BF00374859.
The effect of internal Cl- on the K-ATP channel of pancreatic beta-cells was examined. Reducing Cl- from 140mM to 14mM potentiated channel activity (NPO) approximately 4.5 fold in 60% of patches but was without effect in 40% of patches. The Ki for channel inhibition by ATP was not changed. The inhibitory effect of Cl- interacted with the stimulatory action of MgGDP. In 140mM Cl-, 1mM MgGDP increased NPO in Cl(-)-sensitive patches only: when NPO was potentiated by 14mM Cl-, no further increase was produced by MgGDP. These observations suggest that MgGDP and low Cl- solution may increase channel activity via a similar mechanism.
研究了细胞内氯离子对胰腺β细胞K-ATP通道的影响。将氯离子浓度从140mM降至14mM后，60%的膜片上通道活性（非磷酸化开放概率，NPO）增强了约4.5倍，但40%的膜片无此效应。ATP对通道的抑制常数未改变。氯离子的抑制作用与MgGDP的刺激作用相互影响。在140mM氯离子条件下，1mM MgGDP仅使氯离子敏感的膜片上的NPO增加：当NPO被14mM氯离子增强时，MgGDP不会使其进一步增加。这些观察结果表明，MgGDP和低氯溶液可能通过类似机制增加通道活性。
