Key result
Alterations in endothelial nitric oxide generation and function, potentially due to inactivation by reactive oxygen species, underlie abnormal vascular reactivity in atherosclerosis and vasospasm.
Endothelial dysfunction, particularly the inactivation of nitric oxide by reactive oxygen species, is a key underlying mechanism for abnormal vascular reactivity in atherosclerosis and other vascular diseases.
he importance of the endothelium in regulating vascular tone and reactivity is well recognized.The endothelium produces a variety of substances including nitric oxide (NO), prostaglandins, endothelin-1, and an unidentified hyperpolarization factor that control vascular tone, thrombus formation, platelet and leukocyte adhesion and aggregation, and cellular proliferation.Alterations in the synthesis or activity of these substances appear to play a major role in the pathogenesis of a variety of diseases.Emphasis has been placed on alterations in the generation and function of NO as an underlying mechanism for abnormal vascular reactivity in atherosclerosis and other vascular diseases.Studies in both animal models and humans demonstrate that NO-mediated responses are decreased in atherosclerosis, diabetes, and a wide variety of vascular diseases.But measurements of NO in atherosclerosis have produced variable results with decreases 1 and increases 2 in the levels of NO reported.Inactivation of NO by reactive oxygen species may account for the decrease in NO-mediated responses.
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Kathryn G. Lamping (2002) conducted a review in Vasospasm and atherosclerosis. Nitric oxide (NO) alterations was evaluated. Alterations in endothelial nitric oxide generation and function, potentially due to inactivation by reactive oxygen species, underlie abnormal vascular reactivity in atherosclerosis and vasospasm.
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