Aim To explore the effect of the angiotensin Ⅱ type 1 (AT 1) receptor antagonist irbesartan on cardiomyocytes apoptosis in spontaneous hypertensire rats (SHR),and gain insight into the regulation of cardiac apoptosis. Methods Twenty 13 weeks old SHR were randomly devide into two groups: SHR positive control group,irbesartan treating group [50 mg/(kg·d)],ten normotensive Wistar-Kyoto rats were acted as normal control group. Monitoring blood pressure of rats periodically, After 15 weeks, putting all rats to death, measuring heart weight, then we investigated the changes of cardiomyocytes, apoptosis using in situ TDT-mediated dUTP nick end labeling (TUNEL). The expression of Bcl-2, Bax and P53 was assessed by immunolistochemical detection. Results Compared with WKY, untreated SHR exhibited increased apoptosis (1.59±0.38 vs 0.33±0.11, p<0.01) increased Bax (1.76±0.31 vs 0.59±0.11,p<0.01) and similar Bcl-2(0.88±0.26 vs 0.82±0.19, p>0.05), The Bcl-2/Bax ratio was lower in untreated SHR than in WKY (0.53±0.17 vs 1.41±0.34, p<0.01) . The chronic administration of irbesartan was associated with the the normalization of apoptosis (0.56±0.17 vs 1.59±0.38, p<0.01), Bax expression (0.84±0.23 vs 1.76±0.31, p<0.01) and the Bcl-2/Bax ratio (1.12±0.35 vs 0.53±0.17, p<0.01). No changes in the expression of Bcl-2 were observed in these rats after treatment(0.92±0.28 vs 0.88±0.26,p>0.05). Conclussion Chronic blockade of AT1 receptors prevents Bax overexpression and normalizes apoptosis in the left ventricular of SHR independenty of its hemoclynamic effect. AT1 blocker may prevented apoptosis by acting through a receptor mechanism involving the AT1 receptor, and may participate in the stimulation of Bax protein,which in turn renders cardiomyocytes more susceptible to apoptosis.