title: Ouabain treatment increases nitric oxide bioavailability and decreases superoxide anion production in cerebral vessels.
abstract: OBJECTIVE
  Chronic administration of ouabain induces hypertension and increases the contribution of nitric oxide to vasoconstrictor responses in peripheral arteries. The aim of this study was to analyse whether ouabain treatment alters the nitric oxide bioavailability in cerebral arteries.
  
  
  METHODS
  Basilar arteries from control and ouabain-treated rats ( approximately 8.0 microg/day, 5 weeks) were used. Vascular reactivity was analysed by isometric tension recording, protein expression by western blot, nitric oxide levels by diaminofluorescein-induced fluorescence, superoxide anion (O2) production by ethidium fluorescence and lucigenin chemiluminescence and plasma total antioxidant status by a commercial kit.
  
  
  RESULTS
  The relaxations induced by bradykinin (1 nmol/l-10 micromol/l) and L-arginine (0.01-300 micromol/l) and the contractile responses induced by both N-nitro-L-arginine methyl ester (0.1-100 micromol/l) and oxyhaemoglobin (0.01-10 micromol/l) were greater in arteries from ouabain-treated than control rats. However, the relaxation to diethylamine NONOate-nitric oxide (0.1 nmol/l-10 micromol/l) and the contractions to KCl (7.5-120 mmol/l) and 5-hydroxytryptamine (0.01-10 micromol/l) were similar in arteries from both groups. Ouabain treatment increased basal nitric oxide levels but did not modify endothelial and neuronal nitric oxide synthase protein expression. O2 production was lower in cerebral arteries from ouabain-treated rats; however, plasma total antioxidant status and vascular protein expression of Cu/Zn-superoxide dismutase, Mn-superoxide dismutase and extracellular superoxide dismutase were similar in both groups.
  
  
  CONCLUSIONS
  Chronic ouabain treatment increased nitric oxide basal levels in basilar arteries probably due to the decreased O2 levels. This might be an adaptive mechanism of the cerebral vasculature to the increase in blood pressure.
authors.affiliation: Departamento de Ciencias de la Salud III, Facultad de Ciencias de la Salud, Universidad Rey Juan Carlos, Spain.
authors.forename: Raquel
authors.initials: R
authors.lastname: Hernanz
authors.forename: Ana M
authors.initials: AM
authors.lastname: Briones
authors.forename: Angela
authors.initials: A
authors.lastname: Martín
authors.forename: Amada E
authors.initials: AE
authors.lastname: Beltrán
authors.forename: Teresa
authors.initials: T
authors.lastname: Tejerina
authors.forename: Mercedes
authors.initials: M
authors.lastname: Salaices
authors.forename: María J
authors.initials: MJ
authors.lastname: Alonso
mesh_terms: D000818:Animals; D002536:Cerebral Arteries / Q000187:drug effects* / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D010042:Ouabain / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013481:Superoxides / Q000378:metabolism*; D014661:Vasoconstriction; D014664:Vasodilation
chemical_list: D004791:Enzyme Inhibitors; D013481:Superoxides; D009569:Nitric Oxide; D010042:Ouabain