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Role of cytochrome P-450 metabolites in the regulation of renal function and blood pressure in 2-kidney 1-clip hypertensive rats
Alexandra Sporková, Libor Kopkan, Šárka Varcabová, Zuzana Husková, Sung Hee Hwang, Bruce D. Hammock, John D. Imig, Herbert J. Kramer, Luděk Červenka
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem
Grantová podpora
NS9699
MZ0
CEP - Centrální evidence projektů
NS10499
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
Plný text - Článek
Zdroj
Zdroj
NLK
Open Access Digital Library
od 1997-10-01
- MeSH
- amidiny farmakologie MeSH
- epoxid hydrolasy antagonisté a inhibitory MeSH
- inhibitory enzymů farmakologie MeSH
- krevní tlak účinky léků fyziologie MeSH
- krysa rodu rattus MeSH
- kyseliny arachidonové metabolismus MeSH
- kyseliny hydroxyeikosatetraenové metabolismus MeSH
- ledviny krevní zásobení účinky léků fyziologie MeSH
- modely nemocí na zvířatech MeSH
- regionální krevní průtok účinky léků MeSH
- renovaskulární hypertenze metabolismus patofyziologie MeSH
- sodík moč MeSH
- systém (enzymů) cytochromů P-450 metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
Alterations in renal function contribute to Goldblatt two-kidney, one-clip (2K1C) hypertension. A previous study indicated that bioavailability of cytochrome P-450 metabolites epoxyeicosatrienoic acids (EETs) is decreased while that of 20-hydroxyeicosatetraenoic acids (20-HETE) is increased in this model. We utilized the inhibitor of soluble epoxide hydrolase cis-4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (c-AUCB) and HET-0016, the inhibitor of 20-HETE production, to study the role of EETs and 20-HETE in the regulation of renal function. Chronic c-AUCB treatment significantly decreased systolic blood pressure (SBP) (133 ± 1 vs. 163 ± 3 mmHg) and increased sodium excretion (1.23 ± 0.10 vs. 0.59 ± 0.03 mmol/day) in 2K1C rats. HET-0016 did not affect SBP and sodium excretion. In acute experiments, renal blood flow (RBF) was decreased in 2K1C rats (5.0 ± 0.2 vs. 6.9 ± 0.2 ml·min(-1)·g(-1)). c-AUCB normalized RBF in 2K1C rats (6.5 ± 0.6 ml·min(-1)·g(-1)). HET-0016 also increased RBF in 2K1C rats (5.8 ± 0.2 ml·min(-1)·g(-1)). Although RBF and glomerular filtration rate (GFR) remained stable in normotensive rats during renal arterial pressure (RAP) reductions, both were significantly reduced at 100 mmHg RAP in 2K1C rats. c-AUCB did not improve autoregulation but increased RBF at all RAPs and shifted the pressure-natriuresis curve to the left. HET-0016-treated 2K1C rats exhibited impaired autoregulation of RBF and GFR. Our data indicate that c-AUCB displays antihypertensive properties in 2K1C hypertension that are mediated by an improvement of RBF and pressure natriuresis. While HET-0016 enhanced RBF, its anti-natriuretic effect likely prevented it from producing a blood pressure-lowering effect in the 2K1C model.
Center for Cardiovascular Research Prague
Department of Pharmacology and Toxicology Medical College of Wisconsin Milwaukee Wisconsin
Department of Physiology 2nd Medical Faculty Charles University Prague Czech Republic
Section of Nephrology Medical Policlinic Department of Medicine University of Bonn Bonn Germany
Citace poskytuje Crossref.org
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