Increased apoptosis has been demonstrated recently in the hypertrophied left ventricle of spontaneously 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.Objective:
The changes in pathology and six gene expressions such as caspase-3, Bax, Bcl-2, chemokine receptor (CCR)-2, monocyte chmoattractant protein (MCP)-1and transforming growth factor (TGF) β were investigated to explore the effects of losartan in SHR.Design and Method:
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) for 5 weeks. 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.Results:
Caspase-3, Bcl-2, CCR-2, MCP-1 and 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.Conclusions:
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.