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Possible involvement of free radicals in hypertensive organ injury

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Hypertension is the major risk factor of various kinds of vascular changes and subsequent organ damage. In any kind of vascular change, endothelial injury, not only in large arteries but also in miscovessels, is the most important initial event; so the elucidation of the pathophysiological changes in endothelial cells in hypertension is undoubtedly important for the prevention and treatment the hypertensive patients. In hypertension, although physical stress such as high blood pressure and shear stress is important for endothelial changes, other factors must be involved besides these. Among several factors such as hypercholesterolemia, hyperglycemia, hyperinsulinemia, smoking, and others, free radicals may be a key factor, since a REDOX system could be affected by the above abnormal conditions. Thus, alteration of free radical generation or scavenging ability are essential events for development of hypertension as well as hypertension complications. In a series of experiments to elucidate the pathogenesis of hypertensive vascular injury and its sequelae, we revealed the important role of free radicals in endothelial injury, not only in the aorta but also in brain microvessels. In addition to genetic abnormalities such as mitochondrial DNA alteration, angiotensin II could be an important causative or, at least, stimulating factor of hypertensive endothelial injury. In other words, preexisting hypertension may act as a stimulating factor for free radical injury in the living body.


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