High salt intake increases blood pressure in normal rats

Putative role of 20-HETE and no evidence on changes in renal vascular reactivity

A. Walkowska, M. Kuczeriszka, J. Sadowski, K. H. Olszyñski, L. Dobrowolski, L. Červenka, B. D. Hammock, E. Kompanowska-Jezierska

Research output: Contribution to journalArticle

8 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)323-334
Number of pages12
JournalKidney and Blood Pressure Research
Volume40
Issue number3
DOIs
StatePublished - Jun 23 2015

Fingerprint

Blood Vessels
Salts
Blood Pressure
Kidney
Diet
Acetylcholine
Vasodilator Agents
Norepinephrine
20-hydroxy-5,8,11,14-eicosatetraenoic acid
Epoxide Hydrolases
Benzoic Acid
Renal Circulation
Vasoconstrictor Agents
Renal Artery
Wistar Rats
Lasers
Perfusion
Hypertension
Acids

Keywords

  • 20-HETE
  • High salt diet
  • Hypertension

ASJC Scopus subject areas

  • Nephrology
  • Cardiology and Cardiovascular Medicine

Cite this

Walkowska, A., Kuczeriszka, M., Sadowski, J., Olszyñski, K. H., Dobrowolski, L., Červenka, L., ... Kompanowska-Jezierska, E. (2015). High salt intake increases blood pressure in normal rats: Putative role of 20-HETE and no evidence on changes in renal vascular reactivity. Kidney and Blood Pressure Research, 40(3), 323-334. https://doi.org/10.1159/000368508

High salt intake increases blood pressure in normal rats : Putative role of 20-HETE and no evidence on changes in renal vascular reactivity. / Walkowska, A.; Kuczeriszka, M.; Sadowski, J.; Olszyñski, K. H.; Dobrowolski, L.; Červenka, L.; Hammock, B. D.; Kompanowska-Jezierska, E.

In: Kidney and Blood Pressure Research, Vol. 40, No. 3, 23.06.2015, p. 323-334.

Research output: Contribution to journalArticle

Walkowska, A, Kuczeriszka, M, Sadowski, J, Olszyñski, KH, Dobrowolski, L, Červenka, L, Hammock, BD & Kompanowska-Jezierska, E 2015, 'High salt intake increases blood pressure in normal rats: Putative role of 20-HETE and no evidence on changes in renal vascular reactivity', Kidney and Blood Pressure Research, vol. 40, no. 3, pp. 323-334. https://doi.org/10.1159/000368508
Walkowska, A. ; Kuczeriszka, M. ; Sadowski, J. ; Olszyñski, K. H. ; Dobrowolski, L. ; Červenka, L. ; Hammock, B. D. ; Kompanowska-Jezierska, E. / High salt intake increases blood pressure in normal rats : Putative role of 20-HETE and no evidence on changes in renal vascular reactivity. In: Kidney and Blood Pressure Research. 2015 ; Vol. 40, No. 3. pp. 323-334.
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AU - Kuczeriszka, M.

AU - Sadowski, J.

AU - Olszyñski, K. H.

AU - Dobrowolski, L.

AU - Červenka, L.

AU - Hammock, B. D.

AU - Kompanowska-Jezierska, E.

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N2 - 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.

AB - 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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