DA1 tion noted in the aorta from diabetic animals and in the aorta exposed to elevated glucose may be mediated by free radicals (3 1,40). Superoxide dismutase, a scavenger of superoxide anion, normalized endothelium-dependent relaxations in response to acetylcholine in the aorta of diabetic animals (31, 40). In addition, scavengers of free radicals, including superoxide dismutase, allopurinol, and deferoxamine prevented the impairment of endothelium-dependent relaxation to acetylcholine in control rabbit aortas exposed to elevated glucose (40). The sources of oxygen-derived free radicals in diabetic vessels is not known. A recent report suggests that prostaglandin HZ (PGH2) may inhibit endotheliumdependent relaxations by a mechanism involving formation of superoxide anion (41). Other sources of free radicals in diabetic arteries include the autoxidation of glucose, oxidation of lipids, oxidation of glycosylated proteins, and intracellular production from mitochondria (12, 17, 20, 45). However, information concerning alterations in cell function of the microvasculature is much more limited (l&23). Diabetes-induced cell may serve as a major initiating process leading to the development of diabetic vascular disease involving both large and small arteries. The goals of the present study were to explore the potential role of in the development of diabetic microvascular disease and to
AJP - Heart and Circulatory Physiology – The American Physiological Society
Published: Mar 1, 1994
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