Ionic Remodeling and Direct Effects of Valsartan on Ionic Currentsin Human Atrial Myocytes with Atrial Fibrillation

• 来源期刊: 岭南心血管病杂志（英文版）
• 关键词: Atrial fibrillation Ionic channels Angiotensin receptor antagonist Remodeling
• 年，卷（期）: 2004,（2）
• 页码范围: 63-70
• 页数: 8页
• 语种: 英文

摘要

Objectives Previous studies demonstrated that angiotensin receptor antagonists had effects on some potassium channels in guinea pig myocytes and cloned channels that expressed in human cardiac myocytes. This study determined the direct effects of Valsartan on I caL, INa, IKur, IK1 and Ito1 in isolated human atrial myocytes. Methods and Results Specimens of right atrial appendage tissue were obtained from 39 patients with coronary artery and valvular heart diseases during cardiopulmonary bypass procedure. Pre- operation cardiac rhythm was sinus (SR)in 19 patients and was atrial fibrillation (AF) in the others. Single atrial myocyte was isolated by enzymatic dissociation with the chunk method. The ionic currents were recorded using the whole cell coffiguration of the voltage clamp technique. ICaL and Ito1 densities in AF patients were significantly lower than those in SR patients by 74% and 60%, respectively, while IK1density was significantly higher by 34% at command potential of - 120 mV. With 10 μmol/L Valsartan, INa density was significantly decreased by 59% in SR patients and by 66% in AF patients. IKur and IKl density were significantly decreased in only AF patients by 31% and23%, respectively. Conclusions Conclusions Decreased IcaL and Itol and increased IKl at hyperpolarizing potentials in AF patients' atrial myocytes may result from the electrophysiological remodeling by AF. Valsartan significantly decreases INa, IK1 and IKur current densities in AF patients' myocyte, but decreases only INa in SR patients' myocyte, suggesting that Valsartan may be beneficial to the recovering of remolded atria.