The roles of intrarenal 20-hydroxyeicosatetraenoic and epoxyeicosatrienoic acids in the regulation of renal function in hypertensive Ren-2 transgenic rats
Language English Country Switzerland Media print-electronic
Document type Comparative Study, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't
Grant support
DK38226
NIDDK NIH HHS - United States
HL074167
NHLBI NIH HHS - United States
HL59699
NHLBI NIH HHS - United States
PubMed
17785988
DOI
10.1159/000107710
PII: 000107710
Knihovny.cz E-resources
- MeSH
- Animals, Genetically Modified MeSH
- Hypertension genetics physiopathology MeSH
- Blood Pressure genetics MeSH
- Rats MeSH
- Arachidonic Acids physiology MeSH
- Hydroxyeicosatetraenoic Acids physiology MeSH
- Kidney physiology MeSH
- Rats, Sprague-Dawley MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, N.I.H., Extramural MeSH
- Comparative Study MeSH
- Names of Substances
- 20-hydroxy-5,8,11,14-eicosatetraenoic acid MeSH Browser
- Arachidonic Acids MeSH
- Hydroxyeicosatetraenoic Acids MeSH
BACKGROUND: The present study was performed in hypertensive Ren-2 transgenic rats (TGR) and in normotensive Hannover Sprague-Dawley (HanSD) rats. First, the intrarenal protein expression of CYP4A, the enzyme catalyzing the formation of 20-hydroxyeicosatetraenoic acid (20-HETE), and of CYP2C23, the enzyme responsible for epoxyeicosatrienoic acid (EET) production, was evaluated. Second, the renal functional responses to inhibition of the intrarenal formation of 20-HETE and EETs were investigated. METHODS: Renal hemodynamics and electrolyte excretion were evaluated in response to the administration of inhibitors of 20-HETE and EET formation into the renal artery. In renal cortical tissue, CYP4A and CYP2C23 protein expression was assessed by Western blot analysis. Urinary concentrations of 20-HETE and EETs were measured using a fluorescent HPLC assay. RESULTS: TGR have higher kidney CYP4A protein expression and urinary 20-HETE excretion but significantly lower CYP2C23 protein expression and urinary EET excretion than HanSD. Intrarenal inhibition of 20-HETE and EET formation decreased sodium excretion in HanSD, whereas inhibition of 20-HETE increased urinary excretion of sodium in TGR without altering renal hemodynamics. CONCLUSIONS: Our data suggest that in TGR, deficient intrarenal synthesis of EETs combined with increased synthesis of 20-HETE with its stimulation of tubular sodium absorption may contribute to the development of hypertension in TGR.
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Research on Experimental Hypertension in Prague (1966-2009)
