LOWERING OF PHI INHIBITS CA-2+-ACTIVATED K+ CHANNELS IN PANCREATIC B-CELLS
LOWERING OF PHI INHIBITS CA-2+-ACTIVATED K+ CHANNELS IN PANCREATIC B-CELLS
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DOI：
10.1038/311269a0
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发表时间：
1984-01-01
期刊：
影响因子：
64.8
通讯作者：
FUJIMOTO, WY
中科院分区：
文献类型：
--
作者：
COOK, DL;IKEUCHI, M;FUJIMOTO, WY
胰岛细胞膜的葡萄糖依赖周期性电活动1,2介导钙摄取3,4，这对葡萄糖诱导的胰岛素释放很重要。到目前为止，还没有直接的证据证明将葡萄糖的摄取和代谢与膜电活动的变化联系起来的“第二信使”。最近的证据表明，细胞内酸化以葡萄糖样的方式刺激胰岛b细胞的电活动，这表明代谢产生的质子可能通过阻断K+通道5和使膜去极化来充当信使。因此，质子被认为抑制Ca2+激活的K+电导[GK(Ca)]，而GK(Ca)]被认为产生“起搏器”电流，负责平台去极化和Ca2+尖峰的节律性放电。虽然这些电导通道在一些组织中已被表征为单通道水平[12 - 18]，但它们对细胞内ph的反应知之甚少（文献19），而且它们尚未在b细胞中被表征。因此，我们使用膜片钳方法来研究鉴定的大鼠b细胞，并在这里表明，b细胞GK（Ca）通道被膜去极化和细胞质Ca2+激活，而被细胞质膜表面的酸化抑制。
Glucose-dependent periodic electrical activity of membranes of pancreatic islet cells1,2mediates calcium uptake3,4, which is important for glucose-induced insulin release. As yet there has been no direct evidence identifying the ‘second messenger’ which couples the uptake and metabolism of glucose4to the change of membrane electrical activity. Recent evidence showing that intracellular acidification stimulates islet B-cell electrical activity in a glucose-like manner has suggested that protons produced metabolically may serve as messengers by blocking K+channels5and depolarizing the membrane. Thus protons have been suggested6to inhibit the Ca2+-activated K+-conductance [GK(Ca)] which is thought5–9to produce the ‘pacemaker’ current responsible for the rhythmic firing of plateau depolarizations10and Ca2+spikes11. Although these conductance channels have been characterized at the single channel level in several tissues12–18, little is known of their response to intracellularpH (ref. 19) and they have not yet been characterized in B-cells. We have, therefore, used the patch-clamp method to study identified rat B-cells and show here that the B-cell GK(Ca) channel is activated by membrane depolarization as well as by cytoplasmic Ca2+, while it is inhibited by acidification of the cytoplasmic membrane surface.