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目的:观察AngⅡ对人心房肌细胞膜钙通道电流的影响及卡维地洛的拮抗作用,为应用卡维地洛治疗房性心律失常提供实验基础。方法:急性分离单个人心房肌细胞,采用全细胞膜片钳方法记录L-型钙电流(LCaL)。实验分4组:对照组,AngⅡ(0.1μmol/L)组,卡维地洛(1μmol/L)组,AngⅡ+卡维地洛组。结果:与对照组相比,0.1μmol/LAngⅡ使人心房肌细胞膜LCaL峰值电流密度明显增加(-12.74±1.65vs-5.78±0.82pA/pF,P<0.05)。1μmol/L卡维地洛对人心房肌细胞膜ICa-L无明显影响(-5.72±0.77pA/pF).但可拮抗AngⅡ的作用;AngⅡ+卡维地洛组的ICa-L峰值电流密度(-8.03±0.84pA/pF)与AngⅡ组相比有显著差异(P<0.05)。结论:AngⅡ对人心房肌细胞具有明显的电生理学作用,0.1μmol/LAngⅡ可促进人心房肌细胞膜ICaL.卡维地洛可拮抗AngⅡ对人心房肌细胞膜ICaL的作用。
Objective: To observe the effect of Ang Ⅱ on the calcium channel current in human atrial myocytes and the antagonism of carvedilol, and to provide an experimental basis for the treatment of atrial arrhythmias with carvedilol. Methods: Acutely isolated single atrial myocytes, L-type calcium current (LCaL) was recorded by whole-cell patch-clamp method. The experiment was divided into 4 groups: control group, AngⅡ (0.1μmol / L) group, carvedilol (1μmol / L) group, AngⅡ + carvedilol group. Results: Compared with the control group, the peak current density of LCaL in atrial myocyte increased significantly (P <0.05). 1μmol / L carvedilol had no significant effect on the ICa-L of human atrial myocyte (-5.72 ± 0.77pA / pF), but could antagonize the effect of AngⅡ. The peak current density of ICa-L in AngⅡ + carvedilol group -8.03 ± 0.84pA / pF) compared with AngⅡ group (P <0.05). CONCLUSION: AngⅡ has obvious electrophysiological effects on human atrial myocytes, and 0.1μmol / LAngⅡ can promote ICaL of human atrial myocytes.Carvedilol can antagonize the effect of AngⅡon ICaL of human atrial myocytes.