Proceedings of The Physiological Society
University of Oxford (2011) Proc Physiol Soc 23, PC131
Angiotensin-II-dependent renovascular hypertension and cardiac dysfunction are improved by regular swimming exercise: role of the oxidant-antioxidant balance
Z. N. Özdemir1, S. Özgür2, M. Koç4,1, G. Sener3, B. . Yegen1
1. Physiology, Marmara University School of Medicine, Istanbul, Turkey. 2. Biochemistry, Marmara University School of Pharmacy, Istanbul, Turkey. 3. Pharmacology, Marmara University School of Pharmacy, Istanbul, Turkey. 4. Nephrology, Marmara University School of Medicine, Istanbul, Turkey.
Renovascular hypertension (RVH) remains among the most prevalent causes of secondary hypertension, which develops from activation of the renin-angiotensin system and recruitment of the oxidative stress pathways (Textor, 2009). The impact of physical activity in prevention of renovascular hypertension and oxidative stress has not been elucidated yet. In the present study, the potential protective and therapeutic effects of moderate exercise training (30 min/day 5 days/week swimming for 9 weeks) on the cardiac tissues of Wistar albino rats with experimental RVH were determined. Under ketamine and chlorpromazine (100 and 2 mg/kg, respectively, i.p.) anesthesia 2-kidney-1-clip hypertension was induced as a RVH model with elevated circulating levels of Angiotensin-II. Rats (10-week-old, male, n=55) were divided into 4 groups: sham-operated control, sedentary RVH, post-surgery trained RVH and pre-surgery trained RVH. Echocardiographic imagings were made and the arterial blood pressure (BP) measurements were recorded by tail-cuff method. Rats were decapitated and trunk blood was obtained for the measurement of serum levels of IL-2, IL-6 and TNF-α, while malondialdehyde (MDA), glutathione (GSH) and catalase (CAT) levels and myeloperoxidase (MPO) activity were studied in the cardiac tissue samples. Values are means ± S.E.M., compared by ANOVA. RVH in the sedentary group (173±4.9 mmHg) resulted in increased BP with respect to control group (128±2.1 mmHg; p<0.001). Pre-surgery training prevented the elevation in BP (139±1.4 mmHg; p<0.001), while exercise after the RVH did not alter BP significantly (174±2.8 mmHg). Increased left-ventricular systolic diameter in the sedentary RVH group (4.97±2.3 mm) was decreased in both trained groups (pre-surgery: 3.61±0.19 mm; p<0.05, post-surgery: 3.22±0.17; p<0.01) with respect to control (2.73±0.21mm; p<0.001). The increased levels of serum IL-2, IL-6, TNF-α levels in the sedentary group as compared with the control group (p<0.05) were significantly decreased in pre-surgery trained RVH group (p<0.01). Cardiac MDA levels and MPO activities were increased in the non-exercised RVH group, while training before or after the surgery abolished these elevations (p<0.01). Similarly, depleted GSH and CAT levels in the cardiac tissues of sedentary RVH rats were found to be preserved in both means of exercise (p<0.001). Current results demonstrate that moderate training improves ventricular functions, controls high blood pressure in RVH, while RVH-induced oxidative damage in cardiac tissue is ameliorated through the modulation of oxidant-antioxidant balance. In conclusion, exercise does not only improve the cardiac and circulatory functions, but it also initiates an anti-inflammatory process to defend against the angiotensin-II-induced cardiac injury.
Where applicable, experiments conform with Society ethical requirements