Atrial fibrillation (AF) is the most common sustained arrhythmia encountered in clinical practice.1 Its incidence increases with age and the presence of structural heart disease. It is a major cause of stroke, especially in the elderly. It has been shown that angiotensin converting enzyme inhibitor (ACEI) can reduce the incidence of AF after acute myocardial infarction.2 Several studies have shown that activation of the rennin-angiotensin system is associated with the mechanisms of AF. Irbesartan is a long-acting angiotensin Ⅱ type 1 receptor antagonist used widely in the treatment of hypertension.3 In recent years, it has been demonstrated that patients treated with amiodarone plus irbesartan had a lower rate of recurrence of atrial fibrillation than did patients treated with amiodarone alone.4 These findings suggest that the inhibition of angiotensin Ⅱ may prevent AF, but its underlying electrophysiological mechanisms are obscure. The purpose of this study is to investigate the effects of irbesartan on atrial cell electrophysiology.