Role of Stat3 in the left hypertrophic ventricle in hypertension rats

AIM: To investigate the role of Slat3 in the left hypertrophic ventricle in rats. METHODS: The Goldblatt model of renovascular hypertension was induced in forty - six male Sprague-Dawley rats. The rats were randomized to untreated hypertension group (group H, n=11), spironolactone treatment group (group S, n=12), valsartan treatment group ( group V, n = 11), spironolactone and valsartan treatment group (group S+V, n=11). Ten sham - operated rats served as the control group (group sham, n=10). The tail cuff blood pressure and echocardiogram were detected every week and every other week, respectively. After eight weeks' treatment, the rat left ventricle (LV) was collected. The concentration of angiotensin Ⅱ (Ang Ⅱ ) in LV, the activation of Stat3 and protein expression of c-myc were examined. RESULTS: Ten weeks after operation, LVH was detected in group H and group S (P0.05) but not in group V, S+V and sham. Activation of Stat3 was significantly higher in group H and S than that in group V, S+ V and sham. Activation of Stat3 was positively related to blood pressure, left ventricular mass index, and protein expression of c - myc. CONCLUSION: In the left hypertrophic ventricle of Goldblatt rats, the activation of Stat3 increases significantly. Sustained pressure overload plays an important role in the activation of Stat3. Stat3 may participate in the development and progression of cardiac hypertrophy and is probably a new activator of transcription in signal transduction of cardiac hypertrophy.