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Effects of P1060 and aprikalim on whole-cell currents in rat portal vein; inhibition by glibenclamide and phentolamine.P1060和阿普卡林对大鼠门静脉全细胞电流的影响；格列本脲和酚妥拉明的抑制作用。
Br J Pharmacol. 1993 Apr;108(4):991-8. doi: 10.1111/j.1476-5381.1993.tb13496.x.
2
Properties of diazoxide and cromakalim-induced activation of potassium channels in cultured rat and RINm5F insulin-secreting cells; effects of GTP.二氮嗪和克罗卡林对培养的大鼠及RINm5F胰岛素分泌细胞中钾通道的激活特性；鸟苷三磷酸的作用
Exp Physiol. 1993 Jan;78(1):25-34. doi: 10.1113/expphysiol.1993.sp003668.
3
Purification, characterization, and biosynthesis of margatoxin, a component of Centruroides margaritatus venom that selectively inhibits voltage-dependent potassium channels.珍珠链尾蝎毒液中一种能选择性抑制电压依赖性钾通道的成分——玛格毒素的纯化、特性鉴定及生物合成
J Biol Chem. 1993 Sep 5;268(25):18866-74.
4
Levcromakalim may induce a voltage-independent K-current in rat portal veins by modifying the gating properties of the delayed rectifier.左芬卡尼可能通过改变延迟整流器的门控特性在大鼠门静脉中诱导出一种电压非依赖性钾电流。
Br J Pharmacol. 1993 Nov;110(3):1037-48. doi: 10.1111/j.1476-5381.1993.tb13918.x.
5
Single channel and whole-cell K-currents evoked by levcromakalim in smooth muscle cells from the rabbit portal vein.利沃卡利姆在兔门静脉平滑肌细胞中诱发的单通道和全细胞钾电流。
Br J Pharmacol. 1993 Oct;110(2):583-90. doi: 10.1111/j.1476-5381.1993.tb13850.x.
6
Phosphate and thiophosphate group donating adenine and guanine nucleotides inhibit glibenclamide binding to membranes from pancreatic islets.供体为腺嘌呤和鸟嘌呤核苷酸的磷酸酯和硫代磷酸酯基团可抑制格列本脲与胰岛细胞膜的结合。
Naunyn Schmiedebergs Arch Pharmacol. 1991 Jan;343(1):83-9. doi: 10.1007/BF00180681.

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.

DOI:10.1111/j.1476-5381.1993.tb13955.x
PMID:8306064
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2175876/
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。