Effect of blocking the different links of RAAS on left ventricular remodeling and the expression of protein about apoptosis in goldblatt rat

[Objective] This study was designed to determined whether blockades of aldosterone receptor with spironolactone and angiotensin II receptor with valsartan interfere with the left ventricular(LV) remodeling and the expression of P53,Bax and Bcl-2 in renovascular hypertension rats.[Methods] Two-kidney,one-clip(2K1C) renovascular hypertension was induced in fifty-six male Sprague-Dawley rats.The rats were randomized to untreated hypertension group(group N),spironolactone treatment group(group S).Valsartan treatment group(group V),spironolactone and valsartan treatment group(group S+V).Ten Sham-operated rats served as the control group(group C).After 8 weeks of treatment,the rats were killed and the samples of left ventricle were collected.Left ventricle concentration of angiotensin II(Ang) and aldosterone(ALD) were assessed by radioimmunoassay.Immunohistochemistry was adopted to examine the protein expression of P53,Bax and Bcl-2.[Results]The blood pressure is higher in N group and S group than V,S+V and C groups(P0.05).The immunostained positive for P53 protein can be detected in LV in N group but not in S,V,S+V and C group.The levels of Ang in LV of N group were much higher than the other four groups(P0.05).The levels of ALD in LV of C group were much lower than the other four groups(P0.05),and that of S group was higher than C group.The immunopositivity of Bax in LV in N group was the highest.The Bax/Bcl-2 protein ratio decreased in N group.Immunopositivity of Bax and the protein ratio in V,S+V group was similar with that in C group.[Conclusions]The overload plays the important roles to the development of LVH and the expression of P53,Bax,Bcl-2 protein.Valsartan can inhibit the development of LVH and contribute to systolic dysfunction of Goldblatt Rat.Spironolactone can partly inhibit the development of LVH and contribute to systolic dysfunction of Goldblatt Rat.