Abstract
Exercise training (ExT) is capable of improving the heart function of spontaneously hypertensive rats (SHRs), but the underlying molecular mechanisms remain elusive. This study was aimed to investigate whether inhibition of RhoA/ROCK signaling pathway contributes to the cardiac protection by low-intensity ExT in SHRs. The results demonstrated that, compared with Wistar-Kyoto (WKY) rats, SHRs obviously exhibited higher blood pressure, increased heart weight index and thickness of left ventricular wall, decreased left ventricular function, damaged myocardial construction, and increased collagen fiber of left ventricle (P < 0.05 or P < 0.01). Meanwhile, the mRNA and protein expression levels of RhoA and ROCK in the heart of SHRs were significantly increased, compared with those of WKY rats (P < 0.05 or P < 0.01). Interestingly, the pathological changes of heart aforementioned were all improved in SHR-ExT rats compared with SHR-Sed rats (P < 0.05 or P < 0.01), indicating the cardiac protection of exercise training. In addition, the cardiac protective effect of exercise training could be blocked by LPA, an activator of Rho/ROCK signaling, and the protective effect in SHR rats could be mimicked by Fasudil, an inhibitor of Rho/ROCK signaling. The results strongly suggest that low-intensity ExT can protect heart against structure and function through inhibiting Rho/ROCK signaling pathway in hypertensive rats.