Effects of Valsartan on Ventricular Hypertrophy and Expression of Proline-rich Tyrosine Kinase 2 in Myocardium of Renovascular Hypertensive Rats

Backgroud and Objective Proline-rich tyrosine kinase2(Pyk2) is a Ca~(2+) sensitive,non-receptor tyrosine protein kinase.Previous reports showed Pyk2 involved in development of left ventrieular hypertrophy. The present paper aimed to study the effects of valsartan on ventricular hypertrophy and its effect on the expression of Pyk2 in myocardium in renovascular hypertensive rats(RHR).Methods Two-kidney and one-clip(2K1C) renal hypertensive model was established in Sprague-Dawley rats by chronic partial occlusion of left renal artery,and ran- domized to receive valsartan (30 mg/kg·d) or without treatment for 4 or 8 weeks.Left ventricular mass to body mass ratio was measured.Pyk2 protein expression and phosphorylation was detected by Western blotting.Results Blood pressure,left ventricular mass to body mass ratio,Pyk2 activity in myocardium of RHR were increased gradu- ally.Valsartan reduced BP and prevent myocardial hypertrophy(P0.01).Pyk2 levels and the amount of tyro sine phosphorylated Pyk2 (p-Pyk2) were significantly and progressively increased in hypertrophied myocardium(1 week P0.05;4-12 week P0.01),Valsartan decreased myocardial Pyk2 and p-Pyk2 significantly after 8-12 weeks treatment (P0.01).Conclusion Increased expression of Pyk2 and p-Pyk2 in the left ventricle of RHR is associated with the progression of left ventricular hypertrophy (LVH).Valsartan prevented cardiac hypertrophy in RHR associated with the decrease in Pyk2 expression and its activities in cardiac tissue.