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Inhibition of soluble epoxide hydrolase counteracts the development of renal dysfunction and progression of congestive heart failure in Ren-2 transgenic hypertensive rats with aorto-caval fistula
L. Červenka, V. Melenovský, Z. Husková, P. Škaroupková, A. Nishiyama, J. Sadowski,
Jazyk angličtina Země Austrálie
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
NT14050
MZ0
CEP - Centrální evidence projektů
NT14012
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
Plný text - Článek
Zdroj
Zdroj
NLK
Medline Complete (EBSCOhost)
od 1998-01-01 do Před 1 rokem
PubMed
25969338
DOI
10.1111/1440-1681.12419
Knihovny.cz E-zdroje
- MeSH
- angiotensin I metabolismus MeSH
- angiotensin II metabolismus MeSH
- aorta MeSH
- časové faktory MeSH
- epoxid hydrolasy antagonisté a inhibitory chemie MeSH
- hemodynamika účinky léků MeSH
- inhibitory ACE farmakologie terapeutické užití MeSH
- inhibitory enzymů farmakologie terapeutické užití MeSH
- krevní tlak účinky léků MeSH
- krysa rodu rattus MeSH
- kyseliny mastné mononenasycené metabolismus MeSH
- ledviny účinky léků patofyziologie MeSH
- peptidové fragmenty metabolismus MeSH
- píštěle komplikace MeSH
- potkani transgenní MeSH
- progrese nemoci * MeSH
- renin-angiotensin systém účinky léků MeSH
- renin genetika MeSH
- rozpustnost MeSH
- srdeční frekvence účinky léků MeSH
- srdeční selhání farmakoterapie etiologie patofyziologie MeSH
- systém (enzymů) cytochromů P-450 metabolismus MeSH
- vena cava inferior MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
The detailed mechanisms determining the course of congestive heart failure (CHF) in hypertensive subjects with associated renal dysfunction remain unclear. In Ren-2 transgenic rats (TGR), a model of angiotensin II (ANG II)-dependent hypertension, CHF was induced by volume overload achieved by creation of the aorto-caval fistula (ACF). In these rats we investigated the putative pathophysiological contribution of epoxyeicosatrienoic acids (EETs) and compared it with the role of the renin-angiotensin system (RAS). We found that untreated ACF TGR exhibited marked intrarenal and myocardial deficiency of EETs and impairment of renal function. Chronic treatment of these rats with cis-4-[4-(3-adamantan-1-yl-ureido)cyclohexyloxy]benzoic acid (c-AUCB, 3 mg/L in drinking water), an inhibitor of soluble epoxide hydrolase (sEH) which normally degrades EETs, increased intrarenal and myocardial EETs, markedly improved survival rate, and increased renal blood flow, glomerular filtration rate and fractional sodium excretion, without altering RAS activity. Chronic angiotensin-converting enzyme inhibition (ACEi) with trandolapril, (6 mg/L in drinking water) improved survival rate even more, and also inhibited the development of renal dysfunction; these beneficial actions were associated with significant suppression of the vasoconstrictor/sodium retaining axis and further activation of the vasodilatory/natriuretic axis of the systemic and intrarenal RAS, without modifying tissue availability of biologically active fatty acid epoxides. In conclusion, these findings strongly suggest that chronic sEH inhibition and chronic treatment with ACEi, each of them altering a different vasoactive system, delay or even prevent the onset of decompensation of CHF in ACF TGR, probably by preventing the development of renal dysfunction.
Department of Cardiology Institute for Clinical and Experimental Medicine Prague Czech Republic
Citace poskytuje Crossref.org
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