title: High salt intake increases blood pressure in normal rats: putative role of 20-HETE and no evidence on changes in renal vascular reactivity.
abstract: Background/Aims . High salt (HS) intake may elevate blood pressure (BP), also in animals without genetic salt sensitivity. The development of salt-dependent hypertension could be mediated by endogenous vasoactive agents; here we examined the role of vasodilator epoxyeicosatrienoic acids (EETs) and vasoconstrictor 20-hydroxyeicosatetraenoic acid (20-HETE).
  
  
  METHODS
  In conscious Wistar rats on HS diet systolic BP (SBP) was examined after chronic elevation of EETs using 4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (c-AUCB), a blocker of soluble epoxide hydrolase, or after inhibition of 20-HETE with 1-aminobenzotriazole (ABT). Thereafter, in acute experiments the responses of renal artery blood flow (Transonic probe) and renal regional perfusion (laser-Doppler) to intrarenal acetylcholine (ACh) or norepinephrine were determined.
  
  
  RESULTS
  HS diet increased urinary 20-HETE excretion. The SBP increase was not reduced by c-AUCB but prevented by ABT until day 5 of HS exposure. Renal vasomotor responses to ACh or norepinephrine were similar on standard and HS diet. ABT but not c-AUCB abolished the responses to ACh. Conclusions . 20-HETE seems to mediate the early-phase HS diet-induced BP increase while EETs are not engaged in the process. Since HS exposure did not alter renal vasodilator responses to Ach, endothelial dysfunction is not a critical factor in the mechanism of salt-induced blood pressure elevation.
authors.affiliation: Department of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
authors.forename: A
authors.initials: A
authors.lastname: Walkowska
authors.forename: M
authors.initials: M
authors.lastname: Kuczeriszka
authors.forename: J
authors.initials: J
authors.lastname: Sadowski
authors.forename: K H
authors.initials: KH
authors.lastname: Olszyñski
authors.forename: L
authors.initials: L
authors.lastname: Dobrowolski
authors.forename: L
authors.initials: L
authors.lastname: Červenka
authors.forename: B D
authors.initials: BD
authors.lastname: Hammock
authors.forename: E
authors.initials: E
authors.lastname: Kompanowska-Jezierska
mesh_terms: D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D062186:Arterial Pressure; D001794:Blood Pressure / Q000187:drug effects*; D004851:Epoxide Hydrolases / Q000097:blood; D006893:Hydroxyeicosatetraenoic Acids / Q000037:antagonists & inhibitors / Q000378:metabolism*; D008297:Male; D009569:Nitric Oxide / Q000502:physiology; D009638:Norepinephrine / Q000378:metabolism; D009994:Osmolar Concentration; D051381:Rats; D017208:Rats, Wistar; D012079:Renal Circulation / Q000187:drug effects*; D012982:Sodium, Dietary / Q000009:adverse effects*; D014230:Triazoles / Q000494:pharmacology
chemical_list: D006893:Hydroxyeicosatetraenoic Acids; D012982:Sodium, Dietary; D014230:Triazoles; C033020:1-aminobenzotriazole; D009569:Nitric Oxide; C055987:20-hydroxy-5,8,11,14-eicosatetraenoic acid; D004851:Epoxide Hydrolases; D000109:Acetylcholine; D009638:Norepinephrine