血管紧张素Ⅱ及缬沙坦对犬心房肌细胞外向钾通道电流的作用  

Effects of Angiotensin Ⅱ and Valsartan on outward potassium channel currents in canine atrial myecytes

作　　者：代建军[1] 李广平[2] 李健[2] 许纲[2] 杨万松[2] 

机构地区：[1]济宁医学院附属金乡医院心内科,山东金乡272200 [2]天津医科大学第二医院心脏科

出　　处：《中国医师杂志》2007年第10期1350-1353,共4页Journal of Chinese Physician

摘　　要：目的观察血管紧张素Ⅱ及缬沙坦对犬心房肌细胞外向钾通道电流的作用,探讨其参与房性心律失常的细胞电生理机制。方法急性分离单个犬心房肌细胞,采用全细胞膜片钳方法记录细胞膜快速延迟整流钾电流（Ikr）、缓慢延迟整流钾电流（Iks）、超快速延迟整流钾电流（Ikur）及短暂外向钾电流（Ito）。结果0.5μmol/L AngⅡ可增加Ikr、Iks,抑制Ito,对Ikur无明显影响;5μmol/L缬沙坦对Ikr、Iks、Ikur及Ito均有抑制作用。结论AngⅡ可能通过对外向钾电流的影响促进AF时的AER,缬沙坦作为AT1受体阻滞剂,可改善AF时的AER,对AF有防治作用。Objective To observe the effects of Angiotensin Ⅱ （Ang Ⅱ ） and Valsartan on outward potassium channel currents in canine atrial myocytes and study the mechanisms of Ang Ⅱ and Valsartan on atrial arrhythmia. Methods Single canine atrial myocyte was isolated and whole-cell configuration of the patch-clamp technique was used to detect Ikr, Iks, Ikur and Ito. Results Ang Ⅱ （0. 5 μmol/L） increased Ikr and Iks respectively. Meanwhile, Ang Ⅱ inhibited Ito, but no effect on Ikur. Valsartan （5μmol/L） inhibited Ikr, Iks, Ikur and Ito respectively. Conclusion Ang Ⅱ may promote atrial electrical remodeling of AF by effects of outward potassium currents. As receptor blockers of Angiotensin Ⅱ , Valsartan can prevent atrial electrical remodeling of AF.

关 键 词：血管紧张素Ⅱ 缬氨酸/类似物和衍生物 肌细胞 心脏 钾通道 

分 类 号：R541[医药卫生—心血管疾病]