我们的网站为什么显示成这样?

可能因为您的浏览器不支持样式,您可以更新您的浏览器到最新版本,以获取对此功能的支持,访问下面的网站,获取关于浏览器的信息:

|本期目录/Table of Contents|

大电导钙激活钾通道在高血压病中的研究进展

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2016年第5期
页码:
589-592,600
栏目:
综述
出版日期:
2016-04-25

文章信息/Info

Title:
Research progress of large conductance Ca2+-activated K+ channel in hypertension
作者:
曹乾嫱1付幼林2王云霞3张淑华3罗 骏2
(1.江西省人民医院心内一科,江西 南昌 330000;
2.赣州市人民医院心内科,江西 赣州 341000;
3.江西省人民医院、江西省心血管病研究所,江西 南昌 330000;
Author(s):
CAO Qian-qiang1 FU You-lin2 WANG Yun-xia3 ZHANG Shu-hua3 LUO Jun2
(1.Department of Cardiology, Jiangxi Province People’s Hospital, Nanchang 330000, Jiangxi, China;
2.Department of Cardiology, Ganzhou People’s Hospital, Ganzhou 341000, Jiangxi, China;
3.Jiangxi Provincial Research Institute for Cardiovascular Disease, Nanchang 330000, Jiangxi, China)
关键词:
高血压血管平滑肌细胞离子通道大电导钙激活钾通道
Keywords:
hypertension vascular smooth muscle cell ion channel BKCa channel
分类号:
R544.1
DOI:
-
文献标识码:
A
摘要:
大电导钙激活钾通道(BKCa)是血管平滑肌细胞(VSMCs)上表达最丰富的钾通道,对维持VSMCs的膜电位及血管收缩和舒张的动态平衡具有重要的调节作用。BKCa通道的激活可使细胞膜发生超极化,从而抑制电压依赖性钙通道的激活和钙离子内流,导致平滑肌舒张。对高血压患者的观察和高血压动物模型的研究发现,高血压血管张力升高时平滑肌细胞膜表面钾离子和钙离子通道表达和功能均发生异常,因此,有人推测高血压是离子通道重构导致平滑肌细胞去极化的结果。本文主要综述近年来BKCa通道在高血压病中的研究进展。
Abstract:
Large conductance Ca2+-activated K+ (BKCa) channels are abundantly expressed in vascular smooth muscle cells (VSMCs). Activation of BKCa channels leads to hyperpolarization of the plasma membrane, closure of Ca2+ channels, reduced intracellular Ca2+ levels and eventually vasodilation. Therefore, BKCa channels play an important role in determining membrane potential and regulation of vascular tone. The elevated vascular tone observed in human hypertension and in several experimental models of hypertension points to abnormalities of the expression and function of Ca2+ and/or K+ channels in VSMCs. VSMCs are more depolarized as a consequence of the ‘ion channel remodeling’ that occurs during chronic hypertension. In this review, we will mainly focus on BKCa channels in VSMCs that are reported to be altered in hypertension.

参考文献/References

[1]Carretero OA,Oparil S.Essential hypertension.Part I:definition and etiology[J].Circulation,2000,101(3):329-335.
[2]Nelson MT,Quayle JM. Physiological roles and properties of potassium channels in arterial smooth muscle[J].Am J Physiol,1995,268(4Pt1):C799-C822.
[3]Cox RH,Rusch NJ.New expression profiles of voltage-gated ion channels in arteries exposed to high blood pressure[J].Microcirculation,2002,9(4):243-257.
[4]Harder DR,Brann L,Halpern W.Altered membrane electrical properties of smooth muscle cells from small cerebral arteries of hypertensive rats[J].Blood Vessels,1983,20(3):154-160.
[5]Atkinson NS,Robertson GA,Ganetzky B.A component of calcium-activated potassium channels encoded by the Drosophila slolocus[J].Science, 1991,253 (5019):551-555.
[6]Wang YW,Ding JP,Xia XM,et al.Consequences of the stoichiometry of Slo1 α and auxiliary β subunits on functional properties of large-conductance Ca2+-activated K+ channels[J].J Neurosci,2002,22(5):1550-1561.
[7]Shipston MJ.Alternative splicing of potassium channels:a dynamic switch of cellular excitability[J].Trends Cell Biol,2001,11(9):353-358.
[8]Yan J,Aldrich RW.BK potassium channel modulation by leucinerich repeat-containing proteins[J].Proc Natl Acad Sci USA,2012,109(20):7917-7922.
[9]Hosseinzadeh Z,Almilaji A,Honisch S,et al.Upregulation of the large conductance voltage-and Ca2+-activated K+channels by Janus kinase 2[J].Am J Physiol Cell Physiol,2014,306(11):C1041-C1049.
[10]Toro L,Li M,Zhang Z,et al.MaxiK channel and cell signaling[J].Pflugers Arch,2014,466(5):875-886.
[11]Chen RS,Geng Y,Magleby KL.Mg2+binding to open and closed states can activate BK channels provided that the voltage sensors are elevated[J].J Gen Physiol,2011,138(6):593-607.
[12]Martens JR,Gelband CH.Alterations in rat interlobar artery membrane potential and K+ channels in genetic and nongenetic hypertension[J].Circ Res,1996,79(2):295-301.
[13]England SK,Wooldridge TA,Stekiel WJ,et al.Enhanced single-channel K+current in arterial membranes from genetically hypertensive rats[J].Am J Physiol,1993,264(5Pt2):H1337-1345.
[14]Liu Y,Jones AW,Sturek M. Increased barium influx and potassium current in stroke-prone spontaneously hypertensive rats[J].Hypertension,1994,23 (6Pt2):1091-1095.
[15]Rusch NJ,Runnells AM.Remission of high blood pressure reverses arterial potassium channel alterations[J].Hypertension,1994,23(6Pt2):941-945.
[16]Liu Y,Jones AW,Sturek M. Ca2+-dependent K+ current in arterial smooth muscle cells from aldosterone-salt hypertensive rats[J].Am J Physiol,1995,269(4Pt2):H1246-H1257.
[17]Liu Y,Pleyte K,Knaus HG,et al.Increased expression of Ca2+-sensitive K+ channels in aorta of hypertensive rats[J].Hypertension,1997,30(6):1403-1409.
[18]Liu Y,Hudetz AG,Knaus HG,et al.Increased expression of Ca2+-sensitive K+ channels in the cerebral microcirculation of genetically hypertensive rats:evidence for their protection against cerebral vasospasm[J].Circ Res,1998,82(6):729-737.
[19]Jones AW.Reactivity of ion fluxes in rat aorta during hypertension and circulatory control[J].Fed Proc,1974,33(2):133-137.
[20]Jones AW.Altered ion transport in vascular smooth muscle from spontaneously hypertensive rats.Influences of aldosterone,norepinephrine,and angiotensin[J].Circ Res,1973,33(5):563-572.
[21]Smith JM,Jones AW.Calcium antagonists inhibit elevated potassium efflux from aorta of aldosterone-salt hypertensive rats[J].Hypertension,1990,15(1):78-83.
[22]Rusch NJ,De Lucena RG,Wooldridge TA,et al.A Ca2+-dependent K+ current is enhanced in arterial membranes of hypertensive rats[J].Hypertension,1992,19(4):301-307.
[23]Rusch NJ,Runnells AM.Remission of high blood pressure reverses arterial potassium channel alterations[J].Hypertension,1994,23(6Pt2):941-945.
[24]Asano M,Masuzawa-Ito K,Matsuda T,et al.Functional role of Ca2+-activated K+ channels in resting state of carotid arteries from SHR[J].Am J Physiol,1993,265(3Pt2):H843-H851.
[25]Asano M,Masuzawa-Ito K,Matsuda T,et al.Charybdotoxin-sensitive K+ channels regulate the myogenic tone in the resting state of arteries from spontaneously hypertensive rats[J].Br J Pharmacol,1993,108(1):214-222.
[26]Kolias TJ,Chai S,Webb RC.Potassium channel antagonists and vascular reactivity in strokeprone spontaneously hypertensive rats[J].Am J Hypertens,1993,6(6Pt1):528-533.
[27]Xu H,Bian X,Watts SW,et al.Activation of vascular BK channel by tempol in DOCA salt hypertensive rats[J].Hypertension,2005,46(5):1154-1162.
[28]刘燕锋,王云霞,葛郁芝,等.低温下血压升高对大鼠主动脉平滑肌细胞膜大电导钙激活钾通道的影响[J].中华高血压杂志,2010,18(9):837-840.
[29]Yang Y,Li P-Y,Cheng J,et al.Function of BKCa channels is reduced in human vascular smooth muscle cells from Han Chinese patients with hypertension[J].Hypertension,2013,61(2):519-523.
[30]Nieves-Cintron M,Amberg GC,Nichols CB,et al.Activation of NFATc3 down-regulates the beta1 subunit of large conductance,calcium-activated K+channels in arterial smooth muscle and contributes to hypertension[J].J Biol Chem,2007,282(5):3231-3240.
[31]Amberg GC,Santana LF.Downregulation of the BK channel beta1 subunit in genetic hypertension[J].Circ Res,2003,93(10):965-971.
[32]Amberg GC,Bonev AD,Rossow CF,et al.Modulation of the molecularcomposition of large conductance, Ca2+ activated K+ channels in vascular smooth muscle during hypertension[J].J Clin Invest,2003,112(5): 717-724.
[33]Brenner R,Perez GJ,Bonev AD,et al.Vasoregulation by the beta1 subunit of the calcium-activated potassium channel[J].Nature,2000,407(6806):870-876.
[34]Pluger S,Faulhaber J,Furstenau M,et al.Mice with disrupted BK channel β1 subunit gene feature abnormal Ca21 spark/STOC coupling and elevated blood pressure[J].Circ Res,2000,87(11):E53-E60.
[35]Xu H,Garver H,Galligan JJ,et al.Large-conductance Ca2+-activated K+ channel β1-subunit knockout mice are not hypertensive[J].Am J Physiol Heart Circ Physiol,2011,300(2):H476-H485.
[36]Hu Z,Ma A,Tian H,et al.Effects of age on expression of BKca channel in vascular smooth muscle cells from mesenteric arteries of spontaneously hypertensive rats[J].J Physiol Biochem,2013,69(4):945-955.
[37]Bhattarai Y,Fernandes R,Kadrofske MM,et al.Western blot analysis of BK channel β1-subunit expression should be interpreted cautiously when using commercially available antibodies[J].Physiol Rep,2014,2(10).pii:e12189.

备注/Memo

备注/Memo:
收稿日期: 2015-04-09.
基金项目:国家自然科学基金项目资助(81260065);江西省自然科学基金项目资助(2013BAB205035)
通讯作者:罗骏,主任医师,主要从事冠心病和心律失常基础与临床研究 Email:luojun1966@medmail.com.cn
作者简介:曹乾嫱,主治医师 Email:cqianqiang@163.com
更新日期/Last Update: 2016-04-13