Inhibitory effects of estradiol on inward rectifier and delayed rectifier K+ currents in guinea pig ventricular myocytes.

Zhongguo yao li xue bao = Acta pharmacologica Sinica Pub Date : 1999-07-01

Y Zhang, L L Song, S Z Gu, S G Lu, Z N Zhou

{"title":"Inhibitory effects of estradiol on inward rectifier and delayed rectifier K+ currents in guinea pig ventricular myocytes.","authors":"Y Zhang, L L Song, S Z Gu, S G Lu, Z N Zhou","doi":"","DOIUrl":null,"url":null,"abstract":"Aim: To study the effects of estradiol (Est) on inward rectifier K+ (IK1) and delayed rectifier K+ (IK) channels in isolated guinea pig ventricular myocytes.Methods: Using whole cell patch-clamp recording techniques.Results: Est 10 mumol.L-1 and 100 mumol.L-1 decreased the action potential duration, APD50, from (474 +/- 71) ms to (330 +/- 75) ms and (229 +/- 67) ms (n = 7 cells of 7 guinea pigs, P < 0.05), respectively. Est 100 mumol.L-1 also decreased APD90 from (587 +/- 60) ms to (418 +/- 79) ms (n = 7, P < 0.05). Est inhibited IK tail current (IK.tail) concentration-dependently. IK.tail was depressed 53% (n = 5, P < 0.05) at 10 mumol.L-1 and 80% (n = 5, P < 0.01) at 100 mumol.L-1 compared with control. Est > or = 10 mumol.L-1 blocked IK1. The maximal inhibition of inward current of IK1 occurred at -100 mV test potential was 49% (n = 5, P < 0.01) and outward current of IK1 at -40 mV was 72% (n = 5, P < 0.01). The reverse potential shifted negatively, from -70 to -76 mV.Conclusion: Est possessed blocking effects on both IK1 and IK channels in guinea pig ventricular myocytes.","PeriodicalId":24002,"journal":{"name":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1999-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Zhongguo yao li xue bao = Acta pharmacologica Sinica","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}

引用次数: 0

Abstract

Aim: To study the effects of estradiol (Est) on inward rectifier K+ (IK1) and delayed rectifier K+ (IK) channels in isolated guinea pig ventricular myocytes.

Methods: Using whole cell patch-clamp recording techniques.

Results: Est 10 mumol.L-1 and 100 mumol.L-1 decreased the action potential duration, APD50, from (474 +/- 71) ms to (330 +/- 75) ms and (229 +/- 67) ms (n = 7 cells of 7 guinea pigs, P < 0.05), respectively. Est 100 mumol.L-1 also decreased APD90 from (587 +/- 60) ms to (418 +/- 79) ms (n = 7, P < 0.05). Est inhibited IK tail current (IK.tail) concentration-dependently. IK.tail was depressed 53% (n = 5, P < 0.05) at 10 mumol.L-1 and 80% (n = 5, P < 0.01) at 100 mumol.L-1 compared with control. Est > or = 10 mumol.L-1 blocked IK1. The maximal inhibition of inward current of IK1 occurred at -100 mV test potential was 49% (n = 5, P < 0.01) and outward current of IK1 at -40 mV was 72% (n = 5, P < 0.01). The reverse potential shifted negatively, from -70 to -76 mV.

Conclusion: Est possessed blocking effects on both IK1 and IK channels in guinea pig ventricular myocytes.

本刊更多论文

雌二醇对豚鼠心室肌细胞内向整流和延迟整流K+电流的抑制作用。

目的:研究雌二醇(Est)对离体豚鼠心室肌细胞内向整流K+ (IK1)和延迟整流K+ (IK)通道的影响。方法:采用全细胞膜片钳记录技术。结果:Est 10 μ mol。L-1和100 μ mol。L-1使动作电位持续时间APD50从(474 +/- 71)ms降低到(330 +/- 75)ms和(229 +/- 67)ms (n = 7只豚鼠，P < 0.05)。Est 100 μ mol。L-1使APD90由(587 +/- 60)ms降至(418 +/- 79)ms (n = 7, P < 0.05)。Est抑制IK尾电流(IK.tail)呈浓度依赖性。本土知识。10 μ mol时，尾部下降53% (n = 5, P < 0.05)。L-1和80% (n = 5, P < 0.01)。L-1。Est > or = 10 μ mol。L-1阻断IK1。在-100 mV测试电位下，IK1向内电流抑制率为49% (n = 5, P < 0.01)，在-40 mV测试电位下，IK1向外电流抑制率为72% (n = 5, P < 0.01)。反向电位负移动，从-70 mV到-76 mV。结论:Est对豚鼠心室肌细胞IK1和IK通道均有阻断作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Zhongguo yao li xue bao = Acta pharmacologica Sinica

自引率

0.00%

发文量