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.
出处
《中国医师杂志》
CAS
2007年第10期1350-1353,共4页
Journal of Chinese Physician