title: [Glucocorticoid-induced reduction in NO bioavailability and vascular endothelial dysfunction].
abstract: Glucocorticoid excess enhances superoxide-induced inactivation of nitric oxide (NO) and suppresses NO production through decreasing the expression of endothelial NO synthase. Glucocorticoid-induced decrease in NO bioavailability elicits vasuclar endothelial dysfunction, leading to insufficiency of peripheral circulation, which may be the pathogenesis for idiopathic osteonecrosis of the femoral head (ION) . Glucocorticoid-induced vascular endothelial dysfunction is the major therapeutic target for ION. NO causes overproduction of reactive oxygen species.
authors.affiliation: Tokushima University Hospital, Department of Internal Medicine, Division of Cardiology.
authors.forename: Masashi
authors.initials: M
authors.lastname: Akaike
authors.forename: Toshio
authors.initials: T
authors.lastname: Matsumoto
mesh_terms: D001775:Blood Circulation; D004730:Endothelium, Vascular / Q000201:enzymology / Q000378:metabolism / Q000503:physiopathology*; D005270:Femur Head / Q000098:blood supply; D005271:Femur Head Necrosis / Q000209:etiology*; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D005938:Glucocorticoids; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase