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Introduction:Severe abdominal aortic constriction above the renal arteries induces arterial hypertension above the stenotic site that is the cause of cardiac hypertrophy. Previous studies have shown that high blood pressure induces myocardial oxidative stress with conflicting results. In the present study, we assessed the effects of acute hypertension on the myocardial oxidative stress and its relation with cardiac hypertrophy. Methods:Experiments were performed on two groups of rats, sham and hypertensive (n=5 each group). Rats were made acutely hypertensive by aortic constriction above the renal arteries. After 10 days, the carotid artery pressure of rats was recorded and hearts were removed. Following tissue homogenization, superoxide dismutase (SOD) and catalase (CAT) activities, as well as glutathione (GSH) and malondialdehyde (MDA) levels were determined by biochemical methods in heart tissues. Results:Arterial pressure and cardiac hypertrophy index (heart weight/body weight, g/kg) were increased in hypertensive rats 66% and 74%, respectively. SOD and CAT activity were significantly higher in hypertensive rats (34.42±2.51 and 38.63±4.03 U/mg protein, respectively) compared to sham animals (28.58±0.28 and 23.27±2.13 U/mg protein, respectively). Aortic-banding significantly increased GSH content of myocardium by 47%, and there was not any significant difference in the myocardial MDA between the two groups. Conclusion:The findings of this study indicate that acutely elevated arterial blood pressure induces cardiac hypertrophy concomitant with oxidative stress in rat myocardium. This study also reconfirms that oxidative stress may play an important role in the development of cardiac hypertrophy during hypertension.

Keywords: coarctation, arterial hypertension, oxidative stress, hypertrophy

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