Effects of chronic cytochrome P-450 inhibition on the course of hypertension and end-organ damage in Ren-2 transgenic rats
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem
Grantová podpora
HL5699
NHLBI NIH HHS - United States
PubMed
17604232
DOI
10.1016/j.vph.2007.05.005
PII: S1537-1891(07)00094-8
Knihovny.cz E-zdroje
- MeSH
- cytochrom P-450 CYP2J2 MeSH
- cytochrom P450 CYP4A metabolismus MeSH
- fokálně segmentální glomeruloskleróza patofyziologie MeSH
- heterozygot MeSH
- hypertenze patofyziologie MeSH
- inhibitory cytochromu P450 * MeSH
- inhibitory enzymů farmakologie MeSH
- kardiomegalie patofyziologie MeSH
- kobalt MeSH
- krevní tlak účinky léků MeSH
- krysa rodu Rattus MeSH
- kůra ledviny MeSH
- kyseliny hydroxyeikosatetraenové biosyntéza MeSH
- modely nemocí na zvířatech MeSH
- náhodné rozdělení MeSH
- oxygenasy metabolismus MeSH
- potkani Sprague-Dawley MeSH
- renin-angiotensin systém fyziologie MeSH
- renin genetika metabolismus MeSH
- systém (enzymů) cytochromů P-450 metabolismus MeSH
- triazoly farmakologie MeSH
- vazokonstrikce 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
- Názvy látek
- 1-aminobenzotriazole MeSH Prohlížeč
- 20-hydroxy-5,8,11,14-eicosatetraenoic acid MeSH Prohlížeč
- cobaltous chloride MeSH Prohlížeč
- cytochrom P-450 CYP2J2 MeSH
- cytochrom P450 CYP4A MeSH
- inhibitory cytochromu P450 * MeSH
- inhibitory enzymů MeSH
- kobalt MeSH
- kyseliny hydroxyeikosatetraenové MeSH
- oxygenasy MeSH
- renin MeSH
- systém (enzymů) cytochromů P-450 MeSH
- triazoly MeSH
The aim of the present study was to evaluate the effects of inhibition of cytochrome P-450 (CYP) activity by 1-aminobenzotriazole (ABT) and by CoCl(2), first, on the development of hypertension when treatment was started in young male heterozygous Ren-2 transgenic rats (TGR) and, second, on blood pressure (BP) when treatment was started in adult TGR with established hypertension. Normotensive Hannover Sprague-Dawley (HanSD) rats served as controls. In addition, the renal cortical activities of omega-hydroxylase, the enzyme catalyzing the formation of 20-hydroxyeicosatetraenoic acid (20-HETE), and of epoxygenase, the enzyme responsible for epoxyeicosatrienoic acids (EETs) production, and urinary excretion of 20-HETE and EETs in TGR and HanSD rats were assessed. TGR have higher renal tissue omega-hydroxylase activity and urinary excretion of 20-HETE but have significantly lower renal epoxygenase activity and urinary excretion of EETs than HanSD rats. Treatment of young TGR with ABT and CoCl(2) attenuated the development of hypertension and cardiac hypertrophy and prevented glomerulosclerosis. Administration of ABT and CoCl(2) in adult TGR decreased BP, cardiac hypertrophy, but did not reduce glomerulosclerosis. Our data suggest that altered production and/or action of CYP-derived metabolites play a permissive role in the development and maintenance of hypertension in TGR by enhancing ANG II-induced vasoconstriction.
Citace poskytuje Crossref.org
Research on Experimental Hypertension in Prague (1966-2009)
