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High salt intake increases blood pressure in normal rats: putative role of
20-HETE and no evidence on changes in renal vascular reactivity
#MMPMID26067851
Walkowska A
; Kuczeriszka M
; Sadowski J
; Olszyński KH
; Dobrowolski L
; ?ervenka L
; Hammock BD
; Kompanowska-Jezierska E
Kidney Blood Press Res
2015[]; 40
(3
): 323-34
PMID26067851
show ga
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.
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