Purpose : Increased apoptosis has been demonstrated recently in the hypertrophied left ventricle of spontaneous hypertensive rat (SHR). Although the available evidence suggests that apoptosis can be induced in cardiac cells by a variety of insults including pressure overload, it appears that cardiac apoptosis in adult SHR results from an exaggerated local production of angiotensin. The changes in pathology and six gene expressions such as caspase-3, Bax, Bcl-2, chemokine receptor (CCR)-2, monocyte chemoattractant protein (MCP)-1, transforming growth factor (TGF) β were investigated to explore the effects of losartan in SHR. Methods : Twelve week-old male Wistar rats were grouped as follows: control (C) group, hypertension (H) group and losartan (L) group in which SHR was treated with losartan (10 mg/kg/day). Western blot and reverse transcription polymerase chain reaction analysis were performed. Results: Systolic blood pressure was significantly decreased in the L group compared with the H group in weeks 3 and 5. Caspase-3, Bcl-2, CCR-2, MCP-1, TGF-β genes were significantly increased in the H group compared with the C group in weeks 3 and 5. Caspase-3, MCP-1 and CCR-2 genes were significantly decreased in the L group compared with the H group in week 5. Bcl-2 was significantly decreased in the L group compared with the H group in week 3. Conclusion: Losartan reduced caspase 3, MCP-1, CCR-2 and Bcl-2 gene expressions. Losartan decreased inflammation and apoptosis. Further study is needed for differing doses of losartan in SHR models.