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The renin-angiotensin system (RAS) has been suggested as being an important factor in stress-related responses and as acting as a pro-oxidant in mammals. Studies on antioxidant activity changes in the brain by systemic administration of angiotensin II (Ang II) may provide valuable data, leading to the clarification of the pathogenesis and development of treatment modalities for stress-induced diseases of the body, such as stress-induced hypertension. We examined the antioxidant defense changes in the brain induced by Ang II, by measuring the activities of antioxidant enzymes, including superoxide dismutase (SOD), and the levels of glutathione (GSH) and lipid peroxide (LPO) in the dissected rat brain after subcutaneous injection of human Ang II. The results showed that peripheral administration of Ang II resulted in a decrease in the level of LPO in the cerebral cortex, hippocampus, striatum and hypothalamus of Sprague-Dawley rats. Ang II increased the activities of SOD, glutathione peroxidase and glutathione reductase in the hippocampus and striatum. Borderline-hyper-tensive rats (BHR), a well-known animal model for stress-induced hypertension, showed somewhat different changes in Ang II-induced antioxidant activities compared with those in normal Sprague-Dawley rats (SD). In BHR rats, peripheral administration of Ang II significantly decreased the activities of antioxidant enzymes and the GSH level, but increased the LPO level in various regions of the brain. These results suggested that the oxidative stress induced by Ang II in the brain may be greater in BHR rats than in normal SD rats, and that RAS may constitute an important pathophysiologic factor contributing to stressinduced hypertension in BHR rats.

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