title: Redox control of vascular nitric oxide bioavailability.
abstract: NO is an important component of vascular homeostasis and abnormal NO bioactivity has been implicated in number of disease states with important public health implications. One clear mechanism of impaired NO bioactivity and vascular disease is excess vascular oxidative stress. There is now a wealth of developing data that manipulation of vascular antioxidant stress is the considerable influence of the biologic activity of endothelium-derived NO. It remains to be seen if this influence can be exploited in a manner that truly alters the course of human disease.
authors.affiliation: Evans Memorial Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA.
authors.forename: D T
authors.initials: DT
authors.lastname: Price
authors.forename: J A
authors.initials: JA
authors.lastname: Vita
authors.forename: J F
authors.initials: JF
authors.lastname: Keaney
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001682:Biological Availability; D001808:Blood Vessels / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation; D009566:Nitrates / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D012995:Solubility; D013482:Superoxide Dismutase / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism; D014652:Vascular Diseases / Q000209:etiology / Q000378:metabolism
chemical_list: D000975:Antioxidants; D009566:Nitrates; D013481:Superoxides; C039642:peroxynitric acid; D009569:Nitric Oxide; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase