@misc{Walkowska_Agnieszka_High_2015,
 author={Walkowska, Agnieszka and Kuczeriszka, Marta and Sadowski, Janusz and Olszyński, Krzysztof Hubert and Dobrowolski, Leszek and Cervenka Ludek and Hammock, BD and Kompanowska-Jezierska, Elżbieta},
 editor={Department of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland},
 editor={cDepartment of Entomology and UCD Comprehensive Cancer Center, University of California, Davis, California, USA},
 editor={Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic},
 copyright={Creative Commons Attribution BY-NC 3.0 PL license},
 address={Basel, Switzerland},
 howpublished={online},
 year={2015},
 language={eng},
 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.},
 title={High Salt Intake Increases Blood Pressure in Normal Rats: Putative Role of 20-HETE and No Evidence on Changes in Renal Vascular Reactivity},
 type={Text},
 volume={40},
 number={3},
 journal={Kidney and Blood Pressure Research},
 publisher={Karger},
 keywords={High salt diet, 20-HETE, Hypertension},
}