title: Nitric oxide, nitric oxide synthase, and hypertensive vascular disease.
abstract: In normotension the endothelium produces mainly nitric oxide (NO) and prostacyclin, and the vasodilator and growth inhibitory influence predominates. Hypertension, however, is associated with a shift towards enhanced constriction and vascular hypertrophy. These effects are associated with an apparent decrease in the production of bioactive NO and concomitant increase in the generation of oxygen-derived free radicals, such as superoxide anions (O(2)-). While the enzymatic source of endothelial O(2)- has been debated intensely over the past few years, it may well turn out that the endothelial NO synthase is itself an important producer of O(2)-. Because the redox state of endothelial cells and, for example, the activation of redox-sensitive transcription factors is regulated by the balance between NO and O(2)- production, endothelial NO synthase may well be the most crucial enzyme determining the anti- or prohypertensive and eventually proatherogenic state of the vascular wall.
authors.affiliation: Institut für Kardiovaskuläre Physiologie, Klinikum der J. W. Goethe-Universität, Theodor-Stern-Kai 7, D-60590 Frankfurt am Main, Germany.
authors.forename: R
authors.initials: R
authors.lastname: Busse
authors.forename: I
authors.initials: I
authors.lastname: Fleming
mesh_terms: D000818:Animals; D001161:Arteriosclerosis / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D009569:Nitric Oxide; D019001:Nitric Oxide Synthase