Change of the Janus Kinase-signal Transducer and Activator of Transcription 3 in the Left Hypertrophic Ventricle of Goldblatt rats as well as after Intervention of Valsartan

Objective The aim is to investigate the role of the AT 1 -Stat3 pathway in the development of left ventricular hypertrophy(LVH) of hypertension. Methods The Goldblatt model of renovascular hypertension was induced in 22 male Sprague-Dawley rats which were randomizedto untreated hypertesion group (group H, n =11), valsartan treatment group(group V, n =11, 30 mg/kg·d). Ten nonoperated SD rats were served as control group (group C, n =10). The tail cuff blood pressure was detected every week and echocardiogram was detected every other week. After 10 weeks of operation the rats were sacrificed and left ventricles were collected. Immunohistochemistry was used to examine the activation of Stat3. Left ventricular concentration of Ang Ⅱ was assessed by radioimmunoassay.Results After ten weeks of operation, the blood pressure, meridional end systolic stress (MESS) and LV mass index(LVMI) were elevated in group H than in group C. After 8 weeks treatment of valsartan, BP, MESS, and LVMI in group V were lower significantly than those of group H. Activation of Stat3 and concentration of Ang Ⅱ in left ventricle were greater in group H than that in group C and group V. The activation of Stat3 positively correlated with the SBP, MESS, LVMI and concentration of Ang Ⅱ in the left ventricle. ConclusionIn the development of LVH, Ang Ⅱ in LV and sustained pressure overload may induce Stat3 activation. Furthermore activated Stat3 might feedback and contribute to the production of local Ang Ⅱ. Valsartan inhibit the activation of Stat3, reduce the concentration of Ang Ⅱ in left ventricle and reverse the progression of LVH, suggessting AT 1 -Stat3 is probably a pathway in the signal transduction of left ventricular hypertrophy.