INTRACELLULAR ATP DIRECTLY BLOCKS K+ CHANNELS IN PANCREATIC B-CELLS
INTRACELLULAR ATP DIRECTLY BLOCKS K+ CHANNELS IN PANCREATIC B-CELLS
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DOI：
10.1038/311271a0
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发表时间：
1984-01-01
期刊：
影响因子：
64.8
通讯作者：
HALES, CN
中科院分区：
文献类型：
--
作者：
COOK, DL;HALES, CN
已知葡萄糖诱导的胰腺B细胞去极化1 - 4是由于膜K+渗透性降低5 - 8，并与糖酵解速率增加相关9，但没有直接证据将特定代谢过程或产物与膜K+通道关闭联系起来。在对B细胞中Ca 2+激活的K+通道[GK（Ca）]的质子抑制进行膜片钳研究期间10，我们确定了第二个K+选择性通道，该通道被施加到膜的细胞质表面的ATP快速且可逆地抑制。该通道在离体斑片中具有自发活性，并经常与GK（Ca）通道共存，但对膜电位和细胞内游离Ca ~（2+）和pH不敏感。通道的阻断是ATP特异性的，似乎不需要ATP的代谢。这种ATP敏感性K+通道[GK（ATP）]可能是胰腺B细胞中代谢和膜K+通透性之间的联系。
It is known that glucose-induced depolarization1–4of pancreatic B-cells is due to reduced membrane K+-permeability5–8and is coupled to an increase in the rate of glycolysis9, but there has been no direct evidence linking specific metabolic processes or products to the closing of membrane K+channels. During patch–clamp studies of proton inhibition of Ca2+-activated K+channels [GK(Ca)] in B-cells10, we identified a second K+-selective channel which is rapidly and reversibly inhibited by ATP applied to the cytoplasmic surface of the membrane. This channel is spontaneously active in excised patches and frequently coexists with GK(Ca) channels yet is insensitive to membrane potential and to intracellular free Ca2+andpH. Blocking of the channel is ATP-specific and appears not to require metabolism of the ATP. This ATP-sensitive K+channel [GK(ATP)] may be a link between metabolism and membrane K+-permeability in pancreatic B-cells.