Renal denervation attenuates cardiac hypertrophy in spontaneously hypertensive rats via regulation of autophagy.

Abstract

It has been suggested that renal denervation (RD) may attenuate left ventricular (LV) hypertrophy. However, the role that autophagy serves in this process is currently unclear. In the present study, utilizing a model of hypertension-induced cardiac hypertrophy in spontaneous hypertensive rats, it was demonstrated that RD was significantly associated with a reduction in LV hypertrophy. Furthermore, a decrease in the myocardial mRNA of hypertrophy-associated genes was demonstrated in RD rats compared with sham controls. In addition, RD in hypertension-induced LV hypertrophy rats was associated with the attenuation of cellular autophagic response over activation at a physiological level. This was indicated by a reduction in the expression of Beclin-1, autophagy related 9A and microtubule-associated protein 1A/1B-light chain 3 II/I in RD rats to physiological levels that are observed in control rats. Furthermore, the number of autophagosomes was restored to physiological levels in the cardiomyocytes of RD rats. The results of the current study suggest that RD may attenuate LV hypertrophy via the regulation of autophagic responses.