Effects of valsartan and spironolactone on the expression of c-myc in the left ventricle of renovascular hypertension rats

Objective To assess the roles of the local renin-angiotensin-aldosterone system(RAAS) and mechanical load in the expression of c-myc in hypertrophied myocardium of hypertension.Methods Two-kidney,one-clip(2K1C) renovascular hypertension was induced in Sprague-Dawley rats.The rats were randomized into untreated hypertension group(H group),spironolactone group(gorged spironolactone 50 mg/kg·day,S group),valsartan group(gorged valsartan 30 mg/kg·day,V group),and spironolactone plus valsartan group(gorged spironolactone 50 mg/kg·day and valsartan 30m g/kg·day at the same time,S+V group).Sham-operated rats served as controls(C group).The changes of heart structure and function in all groups were observed with echocardiogram.Left ventricle concentration of angiotensin Ⅱ(AngⅡ) and ALD was assessed by radioimmunoassay.Immunohistochemistry was adopted to examine the protein expression of c-myc.Results After 8 weeks treatment,carotid systolic pressure,MESS(meridian end systolic stress),LVPWd(left ventricular posterior wall thickness at end diastolic),IVSd(interventricular septal thickness at end diastolic) in V group and S+V group were decreased significantly compared with those in H group and S group(P0.05).The left ventricle concentration of AngⅡ was much lower in S group,V group and S+V group than that in H group(p0.05).The expression of c-myc was much higher in H group and S group than that in C group,V group and S+V group(P0.01).The expression of c-myc was positively related to carotid systolic pressure after 8 weeks treatment(r=0.848,P0.01).Significant correlation was also present between MESS and the expression of c-myc(r=0.580,P0.01).No correlation was found between AngⅡ and the expression of c-myc.Conclusion The increasing of mechanical load is an important factor inducing the persistent expression of c-myc in left ventricle cardiomyocytes of renovascular hypertension rats.The persistent expression of protein c-myc is independent on the activating of AngⅡ in left ventricle.