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1、AngⅡ对人心房肌细胞膜钾通道电流的影响及替米沙坦的拮抗作用作者：张殿新，黄岚，王海昌，张荣庆，程何祥，刘兵，张清，郭文怡【关键词】膜片钳术 【Abstract】AIM：ToobservetheeffectsofangiotensinⅡ(AngⅡ)onpotassiumcurrentsofhumanatrialmyocytessoastorevealthemechanismsofatrialarrhythmiainducedbyAngⅡ,andtoprovidealaboratorybasisforthea
2、pplicationofangiotensinⅡreceptorantagonistinthetreatmentofatrialarrhythmias.METHODS:SinglehumanatrialmyocytewasisolatedandtheconventionalwholecellconfigurationofpatchclamptechniquewasusedtodetectmembraneIk1andIto.Theexperimentwasconductedinfourgroups:contro
3、lgroup,AngⅡgroup,telmisartangroup,andAngⅡ+telmisartangroup.RESULTS:Comparedwiththecontrolgroup,AngⅡof0.1μmol/LsignificantlydecreasedthepeakdensityofItoinhumanatrialmyocytes(pA/pF,6.55±0.52vs12.65±1.06,P<0.01).Underthevoltageof-100mV,AngⅡsignificantlyincr
4、easedthepeak13densityofIK1(pA/pF,-9.31±1.02vs-5.23±0.98,P<0.01).Telmisartanof0.01μmol/LhadnosignificanteffectonIk1andItoinhumanatrialmyocytes,butitantagonizedtheeffectsofAngⅡ.InAngⅡ+telmisartangroup,thepeakdensityofIto(pA/pF,11.74±1.28)andthepeakdensityo
5、fIK1(pA/pF,-6.13±1.15)werebothsignificantlydifferentwiththoseinAngⅡgroup（P<0.01）.CONCLUSION:AngⅡhassignificantelectrophysiologicaleffectsonhumanatrialmyocytes.AngⅡof0.1μmol/LsignificantlyincreasesthepeakdensityofIK1,butdecreasesthepeakdensityofItoinhuman
6、atrialmyocytes.TelmisartanantagonizestheeffectsofAngⅡonhumanatrialmyocytes. 【Keywords】telmisartan;potassiumchannels;patchclamptechrieques;heartatria;musclecells;angiotensinⅡ 【摘要】目的：观察AngⅡ对人心房肌细胞膜钾电流的作用，揭示其参与房性心律失常的电生理机制，为应用AngⅡ受体拮抗剂治疗房性心律失常提供实验基础.方法：急性分离单
7、个人心房肌细胞，采用全细胞膜片钳方法记录内向整流钾电流(Ik1)、短暂外向钾电流（Ito）.实验分4组：对照组，AngⅡ（01μmol/L）组，替米沙坦（001μmol/L）组，AngⅡ+替米沙坦组.结果：与对照组相比，01μ13mol/LAngⅡ使人心房肌细胞膜Ito峰值电流密度明显下降(pA/pF,655±052vs1265±106，P＜001）,在-100ｍＶ电压下使IK1峰值电流密度显著升高(pA/pF,-931±102vs-523±098,P<001).0.01μmol/L替米沙坦对人心房肌细
8、胞膜ItoIK1无明显影响，但可拮抗AngII的作用；AngⅡ+替米沙坦组的Ito峰值电流密度(pA/pF,1174±128)和IK1峰值电流密度(pA/pF,-613±115)与AngⅡ组相比有显著差别（P＜001）.结论：AngⅡ对人心房肌细胞具有明显的电生理学作用，01μmol/LAngⅡ可促进人心房肌细胞膜IK1并抑制Ito，替米沙坦可拮抗AngⅡ对人心房肌细胞膜钾电流的作用. 【关键词】
