Abstract

Introduction Oxidative stress and antioxidant activity were determined in leukocytes from 30 hypertensive patients prior to telmisartan treatment and at two months. A control group was evaluated in parallel. Material and methods Mitochondrial membrane potential (Δψ) in leucocytes was evaluated as a marker of oxidative stress. The antioxidant activity was determined by measuring superoxide dismutase (SOD) and catalase (CAT) activity in leukocyte lysates. Results Our results demonstrate enhanced oxidative stress in hypertension as indicated by their increased mitochondrial membrane potential. Activities of leukocyte antioxidant enzymes were also higher in patients at baseline. These results indicate that hypertension leads to oxidative stress with antioxidant enzyme adaptations in order to avoid the negative effect of the oxidation. It is likely that the cellular antioxidant defense systems are capable of adapting to the chronic oxidative stress associated to hypertension. Our observations indicate that there is an increase in oxidative stress that cannot be attributed to a defect in the antioxidant system. Conclusions It can be speculated that when oxidative stress is greater, the cell generates higher antioxidant activity as a defense mechanism. After two month of treatment with telmisartan, hypertension and leukocyte oxidative stress were decreased. Parallelly, a decrease was observed in the antioxidant defense system. This decline suggests that the cells do not need as much antioxidant activity when blood pressure is normalized.

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