High Salt Intake Increases Blood Pressure in Normal Rats: Putative Role of 20-HETE and No Evidence on Changes in Renal Vascular Reactivity

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 va...

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Published in:Kidney & blood pressure research 2015-01, Vol.40 (3), p.323-334
Main Authors: Walkowska, A., Kuczeriszka, M., Sadowski, J., Olszyñski, K.H., Dobrowolski, L., Červenka, L., Hammock, B.D., Kompanowska-Jezierska, E.
Format: Article
Language:English
Subjects:
20-HETE
Acetylcholine - metabolism
Animals
Arterial Pressure
Blood Pressure - drug effects
Epoxide Hydrolases - blood
High salt diet
Hydroxyeicosatetraenoic Acids - antagonists & inhibitors
Hydroxyeicosatetraenoic Acids - metabolism
Hypertension
Male
Nitric Oxide - physiology
Norepinephrine - metabolism
Original Paper
Osmolar Concentration
Rats
Rats, Wistar
Renal Circulation - drug effects
Sodium, Dietary - adverse effects
Triazoles - pharmacology
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Summary: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.
ISSN:1420-4096
1423-0143
DOI:10.1159/000368508