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B细胞中葡萄糖诱导的膜电位变化的离子机制。

Ionic mechanisms of the glucose-induced membrane potential changes in B-cells.

作者信息

Meissner H P, Preissler M

出版信息

Horm Metab Res Suppl. 1980;Suppl 10:91-9.

PMID:6256274
Abstract

The ionic basis of the glucose-induced membrane potential changes in pancreatic B-cells was investigated. The results suggest that the initial depolarization of the membrane in response to a stimulation with glucose is due to a decrease of the K permeability. This depolarization seems to open a voltage-dependent Ca-channel and thereby an additional depolarization, the depolarization phase of the slow waves, is initiated. Insulin release is then triggered by the entering Ca ions. The fast spike activity may be a consequence of the exocytotic process. The polarization phase of the slow waves seems to be caused by the activity of an electrogenic Na-K-pump and a calcium-dependent increase of the K permeability. The activity of the Na-pump is considered to be regulated by the intracellular Na concentration.

摘要

对胰腺β细胞中葡萄糖诱导的膜电位变化的离子基础进行了研究。结果表明,响应葡萄糖刺激时膜的初始去极化是由于钾通透性降低所致。这种去极化似乎打开了电压依赖性钙通道,从而引发了额外的去极化,即慢波的去极化阶段。然后进入的钙离子触发胰岛素释放。快速锋电位活动可能是胞吐过程的结果。慢波的复极化阶段似乎是由电生性钠钾泵的活动以及钾通透性的钙依赖性增加所引起的。钠泵的活动被认为受细胞内钠浓度的调节。

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