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		<identifier>oai:rcin.org.pl:54362</identifier>
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<dc:title xml:lang="en"><![CDATA[High Salt Intake Increases Blood Pressure in Normal Rats: Putative Role of 20-HETE and No Evidence on Changes in Renal Vascular Reactivity]]></dc:title>
<dc:title xml:lang="pl"><![CDATA[High Salt Intake Increases Blood Pressure in Normal Rats: Putative Role of 20-HETE and No Evidence on Changes in Renal Vascular Reactivity]]></dc:title>
<dc:creator><![CDATA[Walkowska, Agnieszka]]></dc:creator>
<dc:creator><![CDATA[Kuczeriszka, Marta]]></dc:creator>
<dc:creator><![CDATA[Sadowski, Janusz]]></dc:creator>
<dc:creator><![CDATA[Olszyński, Krzysztof Hubert]]></dc:creator>
<dc:creator><![CDATA[Dobrowolski, Leszek]]></dc:creator>
<dc:creator><![CDATA[Cervenka Ludek]]></dc:creator>
<dc:creator><![CDATA[Hammock, BD]]></dc:creator>
<dc:creator><![CDATA[Kompanowska-Jezierska, Elżbieta]]></dc:creator>
<dc:creator><![CDATA[Cervenka, Ludek]]></dc:creator>
<dc:subject xml:lang="en"><![CDATA[High salt diet]]></dc:subject>
<dc:subject xml:lang="en"><![CDATA[20-HETE]]></dc:subject>
<dc:subject xml:lang="en"><![CDATA[Hypertension]]></dc:subject>
<dc:subject xml:lang="pl"><![CDATA[High salt diet]]></dc:subject>
<dc:subject xml:lang="pl"><![CDATA[Hypertension]]></dc:subject>
<dc:subject xml:lang="pl"><![CDATA[20-HETE]]></dc:subject>
<dc:description xml:lang="en"><![CDATA[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.]]></dc:description>
<dc:description xml:lang="pl"><![CDATA[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.]]></dc:description>
<dc:publisher><![CDATA[Karger]]></dc:publisher>
<dc:contributor><![CDATA[Department of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland]]></dc:contributor>
<dc:contributor><![CDATA[cDepartment of Entomology and UCD Comprehensive Cancer Center, University of California, Davis, California, USA]]></dc:contributor>
<dc:contributor><![CDATA[Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic]]></dc:contributor>
<dc:contributor><![CDATA[aDepartment of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland]]></dc:contributor>
<dc:contributor><![CDATA[bCenter for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic]]></dc:contributor>
<dc:date><![CDATA[2015]]></dc:date>
<dc:type xml:lang="en"><![CDATA[Text]]></dc:type>
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<dc:identifier><![CDATA[https://rcin.org.pl/dlibra/publication/74616/edition/54362/content]]></dc:identifier>
<dc:identifier><![CDATA[oai:rcin.org.pl:54362]]></dc:identifier>
<dc:language><![CDATA[eng]]></dc:language>
<dc:relation><![CDATA[Kidney and Blood Pressure Research]]></dc:relation>
<dc:relation><![CDATA[oai:rcin.org.pl:publication:74616]]></dc:relation>
<dc:relation><![CDATA[Kidney and blood pressure research]]></dc:relation>
<dc:rights xml:lang="en"><![CDATA[Creative Commons Attribution BY-NC 3.0 PL license]]></dc:rights>
<dc:rights xml:lang="pl"><![CDATA[Licencja Creative Commons Uznanie autorstwa-Użycie niekomercyjne 3.0 Polska]]></dc:rights>
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