Regular swimming exercise performed either before or after the induction of renovascular hypertension alleviates oxidative renal injury in rats

Abstract

Epidemiological studies have shown that regular exercise and increased aerobic fitness are associated with a decrease in allcause mortality and morbidity, including diseases related with high blood pressure. However, whether exercise has an antiinflammatory impact on the pathogenesis of hypertension was not elucidated yet. In the present study, to investigate the potential protective and therapeutic effects of exercise training (swimming for 30 min/day, 5 days/week for 9 weeks) on renovascular hypertension (RVH) 10-week-old male Wistar albino rats were divided into 4 groups as sham-operated sedentary control group, sedentary group with RVH (2-Kidney, 1-Clip Goldblatt) and two exercised RVH groups, which had 9-week training either before the surgery or after the surgery. Systolic blood pressures (SBP) were measured by the tail-cuff method on a weekly basis and at the end of 12 weeks, rats were decapitated to obtain kidneys. SBP were significantly higher in the sedentary RVH group than the control group, whereas in the trained RVH group measurements were not different than those of the control animals. In the renal tissues of the sedentary RVH group, malondialdehyde and myeloperoxidase levels were increased with a concomitant decrease in glutathione levels, while in the trained RVH group the levels were not different than those of the control group. Moreover, in the trained RVH group, superoxide dismutase and catalase levels measured as antioxidant parameters, were also significantly increased as compared with those of the sedentary RVH group. Current results demonstrate that regular moderate training controls high blood pressure in RVH, while RVH-induced oxidative damage in renal tissue is ameliorated through the modulation of oxidant-antioxidant balance. Exercise training does not only improve the circulatory functions, but it also initiates an anti-inflammatory process to defend against the angiotensin-II-induced renal injury.