Title:

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

Creator:

Walkowska, Agnieszka ; Kuczeriszka, Marta ; Sadowski, Janusz ; Olszyński, Krzysztof Hubert ; Dobrowolski, Leszek ; Cervenka, Ludek ; Hammock, BD ; Kompanowska-Jezierska, Elżbieta

Contributor:

aDepartment of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland ; bCenter for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic ; cDepartment of Entomology and UCD Comprehensive Cancer Center, University of California, Davis, California, USA

Publisher:

Karger

Place of publishing:

Basel,Switzerland

Date issued/created:

2015

Type of object:

Czasopismo/Artykuł

Subject and Keywords:

High salt diet ; Hypertension ; 20-HETE

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. © 2015 S. Karger AG, Basel.

Relation:

Kidney and blood pressure research

Volume:

40

Issue:

3

Start page:

323

End page:

334

Resource type:

Tekst

Detailed Resource Type:

Artykuł

Format:

text/xml

Language:

eng

Rights:

Licencja Creative Commons Uznanie autorstwa-Użycie niekomercyjne 3.0 Polska

Terms of use:

Zasób chroniony prawem autorskim. [CC BY-NC 3.0 PL] Korzystanie dozwolone zgodnie z licencją Creative Commons Uznanie autorstwa-Użycie niekomercyjne 3.0 Polska, której pełne postanowienia dostępne są pod adresem: ; -

Digitizing institution:

Mossakowski Medical Research Institute PAS

Original in:

Biblioteka Instytutu Medycyny Doświadczalnej i Klinicznej im. M. Mossakowskiego PAN

Access:

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