Effect Of Grape Seed Procyanidins On The Cardiac Hypertrophy In Renovascular Hypertensive Rats And Its Mechanism

Objective:To study the effect of grape seed procyanidins (GSP) on the cardiac hypertrophy in renovascular hypertensive (RH) rats and explore its mechanism.Methods:In this experiment, we used two kidney one clip method to establish the RH rat models of myocardial hypertrophy. After2weeks of operation, we selected32rats which tail systolic pressure increased above130mmHg as successful RH rats. The rats were randomly assigned to4groups:RH model group; low dose GSP treatment group (low GSP,50mg·kg-1·d-1); high dose GSP treatment group (high GSP,200mg·kg-1·d-1) and positive control group treated with captopril (captopril,30mg·kg-1·d-1). Meanwhile, sham operation group was set up. Six weeks later, the heart weight/body weight (HW/BW) and left ventricle weight/body weight (LVW/BW) were measured and the myocardial cells histological changes were investigated. The content of hydroxyproline, type Ⅰ, Ⅲ collagen and angiotensin Ⅱ in the left ventricular tissue were determined respectively. SOD activity, MDA and NO content were assayed. Western blotting was used to evaluate the expressions of endothelial nitric oxide synthase, endothlin-1and phosphorylated extracelluar signal-regulated kinase1/2in the left ventricular tissue.Results:Compared with sham operation group, the tail systolic pressure, myocardial hypertrophy index, and the myocardial cross-section area in RH model group were increased significantly(P<0.05). In the RH model rats, treatment with GSP reduced the tail systolic pressure, myocardial hypertrophy index, the myocardial cross-section area, and the content of hydroxyproline, type Ⅰ, Ⅲ collagen, angiotensin Ⅱ, as well as the protein expression of ET-1and phosphorylated extracelluar signal-regulated kinase1/2in myocardial tissue, increased SOD activity, NO content and the expressions of eNOS in myocardial tissue. Its treatment effect is equal to captopril’s.Conclusion:GSP has the obvious inhibitory action on the cardiac hypertrophy in the RH rats by reducing the tail systolic pressure, the content of angiotensin Ⅱ in myocardial tissue, increasing the antioxidative ability, the expressions of eNOS and NO production, and inhibiting the expressions of ET-1, as well as the activation of ERK/MAPK signal transduction pathway.