通过对大鼠门静脉胰岛素瘤细胞中延迟整流通道进行修饰来诱导格列本脲敏感的钾电流。
Induction of a glibenclamide-sensitive K-current by modification of a delayed rectifier channel in rat portal vein in insulinoma cells.
作者信息
Edwards G, Weston A H
机构信息
Department of Physiological Sciences, University of Manchester.
出版信息
Br J Pharmacol. 1993 Dec;110(4):1280-1. doi: 10.1111/j.1476-5381.1993.tb13955.x.
Abstract
In insulinoma cells (RINm5F), the glibenclamide-sensitive K-current (IK(ATP)) which developed spontaneously or after exposure to levcromakalim or to butanedione monoxime was always accompanied by a reduction in the delayed rectifier current (IK(V)). At potentials over which IK(V) was fully activated, the total outward current remained constant. In rat portal vein, the delayed rectifier channel inhibitor, margatoxin, reduced the combined induction of IK(ATP) and inhibition of IK(V) by levcromakalim. These data suggest that the ATP-sensitive K-channel, K(ATP), is a voltage-insensitive state of the delayed rectifier, KV.
摘要
在胰岛素瘤细胞（RINm5F）中，自发形成的或在暴露于左卡尼汀或丁二酮单肟后产生的格列本脲敏感钾电流（IK(ATP)）总是伴随着延迟整流电流（IK(V)）的减少。在IK(V)完全激活的电位下，总外向电流保持恒定。在大鼠门静脉中，延迟整流通道抑制剂玛格毒素减少了左卡尼汀对IK(ATP)的联合诱导和对IK(V)的抑制。这些数据表明，ATP敏感钾通道K(ATP)是延迟整流钾通道KV的一种电压不敏感状态。
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