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 language | English (US) |
|---|---|
| Pages (from-to) | 323-334 |
| Number of pages | 12 |
| Journal | Kidney and Blood Pressure Research |
| Volume | 40 |
| Issue number | 3 |
| DOIs | |
| State | Published - Jun 23 2015 |
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Keywords
- 20-HETE
- High salt diet
- Hypertension
ASJC Scopus subject areas
- Nephrology
- Cardiology and Cardiovascular Medicine
Cite this
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 journal › Article
}
TY - JOUR
T1 - High salt intake increases blood pressure in normal rats
T2 - Putative role of 20-HETE and no evidence on changes in renal vascular reactivity
AU - Walkowska, A.
AU - Kuczeriszka, M.
AU - Sadowski, J.
AU - Olszyñski, K. H.
AU - Dobrowolski, L.
AU - Červenka, L.
AU - Hammock, B. D.
AU - Kompanowska-Jezierska, E.
PY - 2015/6/23
Y1 - 2015/6/23
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.
KW - 20-HETE
KW - High salt diet
KW - Hypertension
UR - http://www.scopus.com/inward/record.url?scp=84930921499&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84930921499&partnerID=8YFLogxK
U2 - 10.1159/000368508
DO - 10.1159/000368508
M3 - Article
VL - 40
SP - 323
EP - 334
JO - Kidney and Blood Pressure Research
JF - Kidney and Blood Pressure Research
SN - 1420-4096
IS - 3
ER -