Different mechanisms of acute versus long-term antihypertensive effects of soluble epoxide hydrolase inhibition: studies in Cyp1a1-Ren-2 transgenic rats
Jazyk angličtina Země Austrálie Médium print
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem
Grantová podpora
HL59699
NHLBI NIH HHS - United States
R01 HL059699
NHLBI NIH HHS - United States
P01 DK038226
NIDDK NIH HHS - United States
R01 ES013933
NIEHS NIH HHS - United States
R01 ES002710
NIEHS NIH HHS - United States
P42ES013933
NIEHS NIH HHS - United States
P42 ES004699
NIEHS NIH HHS - United States
U24 DK097154
NIDDK NIH HHS - United States
DK38226
NIDDK NIH HHS - United States
R37 ES002710
NIEHS NIH HHS - United States
R01 ES02710
NIEHS NIH HHS - United States
PubMed
25224811
PubMed Central
PMC4347520
DOI
10.1111/1440-1681.12310
Knihovny.cz E-zdroje
- Klíčová slova
- angiotensin-II, cytochrome P-450 epoxygenase, eicosanoids, epoxyeicosatrienoic acids, hypertension, soluble epoxide hydrolase,
- MeSH
- angiotensin II metabolismus MeSH
- antihypertenziva farmakologie MeSH
- cytochrom P-450 CYP1A1 metabolismus MeSH
- epoxid hydrolasy antagonisté a inhibitory metabolismus MeSH
- hypertenze farmakoterapie metabolismus MeSH
- indoly metabolismus MeSH
- krevní tlak účinky léků MeSH
- krysa rodu Rattus MeSH
- ledviny účinky léků metabolismus MeSH
- myši MeSH
- natriuréza účinky léků MeSH
- potkani inbrední F344 MeSH
- potkani transgenní MeSH
- renin-angiotensin systém účinky léků MeSH
- renin metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
- Názvy látek
- angiotensin II MeSH
- antihypertenziva MeSH
- cytochrom P-450 CYP1A1 MeSH
- epoxid hydrolasy MeSH
- indole-3-carbinol MeSH Prohlížeč
- indoly MeSH
- Ren2 protein, rat MeSH Prohlížeč
- renin MeSH
Recent studies have shown that the long-term antihypertensive action of soluble epoxide hydrolase inhibition (sEH) in angiotensin-II (AngII)-dependent hypertension might be mediated by the suppression of intrarenal AngII levels. To test this hypothesis, we examined the effects of acute (2 days) and chronic (14 days) sEH inhibition on blood pressure (BP) in transgenic rats with inducible AngII-dependent hypertension. AngII-dependent malignant hypertension was induced by 10 days' dietary administration of indole-3-carbinol (I3C), a natural xenobiotic that activates the mouse renin gene in Cyp1a1-Ren-2 transgenic rats. BP was monitored by radiotelemetry. Acute and chronic sEH inhibition was achieved using cis-4-(4-(3-adamantan-1-yl-ureido)cyclohexyloxy) benzoic acid, given at doses of 0.3, 3, 13, 26, 60 and 130 mg/L in drinking water. At the end of experiments, renal concentrations of epoxyeicosatrienoic acids, their inactive metabolites dihydroxyeicosatrienoic acids and AngII were measured. Acute BP-lowering effects of sEH inhibition in I3C-induced rats was associated with a marked increase in renal epoxyeicosatrienoic acids to dihydroxyeicosatrienoic acids ratio and acute natriuresis. Chronic treatment with cis-4-(4-(3-adamantan-1-yl-ureido)cyclohexyloxy) benzoic acid in I3C-induced rats elicited dose-dependent persistent BP lowering associated with a significant reduction of plasma and kidney AngII levels. Our findings show that the acute BP-lowering effect of sEH inhibition in I3C-induced Cyp1a1-Ren-2 transgenic rats is mediated by a substantial increase in intrarenal epoxyeicosatrienoic acids and their natriuretic action without altering intrarenal renin-angiotensin system activity. Long-term antihypertensive action of cis-4-(4-(3-adamantan-1-yl-ureido)cyclohexyloxy) benzoic acid in I3C-induced Cyp1a1-Ren-2 transgenic rats is mediated mostly by suppression of intrarenal AngII concentration.
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Epoxyeicosanoids in hypertension