Object

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

Contributor:

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

Publisher:

Karger

Place of publishing:

Basel, Switzerland

Abstract:

Abstrakt 0 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.

Relation:

Kidney and Blood Pressure Research

Volume:

40

Issue:

3

Start page:

323

End page:

334

Format:

text/xml

Resource Identifier:

oai:rcin.org.pl:54362

Language:

eng

Rights:

Creative Commons Attribution BY 3.0 PL license

Terms of use:

Copyright-protected material. [CC BY 3.0 PL] May be used within the scope specified in Creative Commons Attribution BY 3.0 PL license, full text available at:

Digitizing institution:

Mossakowski Medical Research Center PAS

Original in:

Library of the Mossakowski Medical Research Center PAS

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