Effects of angiotensin AT_1 receptor antagonist,valsartan,on cardiac remodeling and left ventricular dysfunction after myocardial infarction in rats

Objective:To assess the cardioprotective effects of a novel angiotensin AT 1 receptor antagonist,valsartan,in rats with myocardial infarction.Methods:Male Wistar rats that underwent coronary ligation were randomized to receive valsartan treatment(30 mg/kg) or placebo(physiological saline,1 ml/kg) 1 day after myocardial infarction. Treatment was continued up to 6 weeks after myocardial infarction. Sham operation rats served as controls. Mean arterial blood pressure(MAP),maximum rate of rise of the left ventricular pressure(dP/dt max ),left ventricular end diastolic pressure(LVEDP),inner diameter and circumference of left ventricle,septal thickness,infarct size,interstitial collagen and heart weight,heart weight to body weight ratio were measured at the end of the treatment.Results:Myocardial infarction induced cardiac hypertrophy,interstitial collagen deposition and left ventricular dilatation,and impaired left ventricular function. Valsartan treatment decreased heart weight and heart weight to body weight ratio,diminished interstitial collagen content,lowered LVEDP,and improved myocardial contractility(all P0.05～0.01) compared to that of placebo treated infarct rats.Conclusion:The present results demonstrate that chronic treatment with the angiotensin AT 1 receptor antagonist valsartan can attenuate cardiac structural remodeling and improve left ventricular dysfunction after myocardial infarction in rats.