title: Short-term hypercaloric diet induces blunted aortic vasoconstriction and enhanced vasorelaxation via increased nitric oxide synthase 3 activity and expression in Dahl salt-sensitive rats.
abstract: OBJECTIVE
  To elucidate the role of the O(2)(-), H(2)O(2) or NO pathways in aortic angiotensin (Ang)II-induced vasoconstriction in Dahl salt-sensitive (SS) rats compared with control SS-13(BN) rats on a normal or hypercaloric diet.
  
  
  METHODS
  Aortic function was assessed using wire myography in 16-week-old rats maintained on a normal diet or a 4-week hypercaloric diet. Nitric oxide synthase (NOS) activity and expression was determined by the conversion of radio-labelled arginine to citrulline and Western blot analysis respectively.
  
  
  RESULTS
  On normal diet, AngII-induced vasoconstriction was greater in SS than SS-13(BN) rats. Polyethylene glycol superoxide dismutase (PEG-SOD) reduced the aortic AngII response similarly in both strains on normal diet. Catalase blunted, whereas N(ω)-Nitro-L-arginine methyl ester (L-NAME) did not affect the AngII response in SS rats. In SS-13(BN) rats, catalase had no effect and L-NAME enhanced AngII response. On hypercaloric diet, aortic AngII responsiveness was reduced in SS but unaltered in SS-13(BN) rats compared with their normal diet counterparts. PEG-SOD reduced the AngII response in both rats on hypercaloric diet. Catalase treatment did not alter aortic AngII response, while L-NAME increased the response in SS rats on hypercaloric diet. In SS-13(BN) rats on hypercaloric diet, catalase reduced and L-NAME did not alter the AngII response. Furthermore, aortic endothelial-dependent vasorelaxation was increased in SS rats on hypercaloric diet compared with normal diet and aortic NOS3 activity and expression was increased.
  
  
  CONCLUSIONS
  A short-term hypercaloric diet induces a blunted vasoconstrictive and enhanced vasodilatory phenotype in SS rats, but not in SS-13(BN) rats, via reduced H(2)O(2) and increased NOS3 function.
authors.affiliation: Section of Experimental Medicine, Department of Medicine, Medical College of Georgia, Georgia Health Sciences University, Augusta, GA 30912, USA.
authors.forename: F T
authors.initials: FT
authors.lastname: Spradley
authors.forename: K-T
authors.initials: KT
authors.lastname: Kang
authors.forename: J S
authors.initials: JS
authors.lastname: Pollock
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism* / Q000503:physiopathology; D015153:Blotting, Western; D004032:Diet / Q000009:adverse effects*; D002149:Energy Intake; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D051381:Rats; D020303:Rats, Inbred Dahl; D014661:Vasoconstriction / Q000502:physiology*; D014664:Vasodilation / Q000502:physiology*
chemical_list: D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat