Varied causative and risk factors can lead to cardiac dysfunction. Cardiac dysfunction often evolves into heart failure by cardiac remodeling due to autonomic nervous system disturbance and neurohumoral abnormalities, even if the detriment factors are removed. Renal sympathetic nerve activity plays a pivotal regulatory role in neurohumoral mechanisms. The present study was designed to determine the therapeutic eff ects of renal sympathetic denervation (RSD) on cardiac dysfunction, fibrosis, and neurohumoral response in transverse aortic constriction (TAC) rats with chronic pressure overload. The present study demonstrated that RSD attenuated myocardial fibrosis and hypertrophy, and structural remodeling of the left atrium and ventricle, up -regulated cardiac β adrenoceptor (β -AR, including β 1 AR and β 2 AR) and sarco -endoplasmic reticulum Ca 2+ -ATP ase (SERCA) while down -regulated angiotensin II type 1 receptor (AT 1 R), and decreased plasma B -type natriuretic peptide (BNP), norepinephrine (NE) , angiotensin II (Ang II), and arginine vasopressin (AVP) levels in TAC rats with chronic pressure overload. We conclude that RSD attenuates myocardial fibrosis, the left atrial enlargement, and the left ventricular wall hypertrophy; inhibits the overdrive of the sympathetic ner vous system (SNS), renin- angiotensin -aldosterone system (RAAS), and AVP system in TAC rats with chronic pressure overload . RSD could be a promising non -pharmacological approach to control the progression of cardiac dysfunction., Z.-Z. Li, H. Jiang, D. Chen, Q. Liu, J. Geng, J.-Q. Guo, R.-H. Sun, G.-Q. Zhu, Q.-J. Shan., and Obsahuje bibliografii