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Pressure lowering effect of chronic exercise mediated by reduced myocardial pro‐inflammatory cytokines and oxidative stress in hypertensive rats
Author(s) -
Agarwal Deepmala,
Haque Masudul,
Sriramula Srinivas,
Mariappan Nithya,
Francis Joseph
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.1017.9
Subject(s) - oxidative stress , medicine , blood pressure , superoxide , reactive oxygen species , endocrinology , nadph oxidase , cardiac function curve , cardiology , heart rate , muscle hypertrophy , chemistry , heart failure , biochemistry , enzyme
Beneficial effects of physical activity on hypertension are well known, however the precise mechanisms of exercise in early stage of hypertension are poorly understood. Therefore, we hypothesized that chronic moderate intensity exercise would reduce myocardial oxidative stress and pro‐inflammatory cytokines (PICs) in hypertensive rats, thereby contributing to lowered blood pressure and improved cardiac function. Young normotensive (WKY) and hypertensive rats (SHR) were given moderate intensity exercise for 15 weeks. Blood pressure was measured by tail‐cuff system. Cardiac function was assessed by echocardiography. Myocardial total reactive oxygen species (ROS) and superoxide production was estimated by Electron Paramagnetic Resonance method. Real time‐PCR was used for determination of PICs and NADPH oxidase genes. Chronic exercise caused a significant reduction in blood pressure in SHR. Trained SHR showed decreased left ventricular mass index, relative wall thickness and Tei index indicating reduced concentric hypertrophy and improved cardiac function. Exercise training caused a significant reduction of PICs, NOX2 and iNOS in SHR which was associated with attenuated total ROS and superoxide production. In summary, exercise exerts its beneficial effects by decreasing oxidative stress and PICs. Grant support: National Heart, Lung and Blood Institute grant HL‐80544 for Dr. Joseph Francis.