| Background and ObjectiveLeft ventricular hypertrophy is an independent risk factor of cardiovascular disease. In the development of left ventricular hypertrophy cardiac remodeling occurs, cardiac remodeling consists a series of the changes of contents and structures of myocardial extracelluar matrix. The rate limiting step in the extracellular degradation of collagen is the catalytic cleavage by interstitial matrix metalloproteinases(MMPs). The MMP activity is regulated by a family of naturally occurring tissue inhibitors of metalloproteinases (TIMPs). The balance between MMPs and TIMPs is a critical factor of degradation of extracellular matrix. Candesartan is a new angiotensin II receptor blocker and acts as therapy of primary hypertension. It can inhibit cardiac hypertrophy. Whether or not candesartan can influence cardiac remodeling and what the mechanism are not clear. This study initially investigates the roles of MMP-13/TIMP-1 system on cardiac remodeling and the effects and possible mechanisms of candesartan on left ventricular hypertrophy(LVH) induced by norepinephrine(NE).Materials and Methods29 female Wistar rats were randomly divided into three groups: control group(n=10), NE group(n=9) and NE+candesartan group(n=10). The rats were intraperitoneal injected either normal sodium(control group), or NE(2.4 mg·kg-1·d-1 ) (NE group and NE+candesartan group) twice a day for 15 days. The rats were... |