Orally active epoxyeicosatrienoic acid analog does not exhibit antihypertensive and reno- or cardioprotective actions in two-kidney, one-clip Goldblatt hypertensive 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
DK38226
NIDDK NIH HHS - United States
PubMed
26304700
DOI
10.1016/j.vph.2015.08.013
PII: S1537-1891(15)00199-8
Knihovny.cz E-zdroje
- Klíčová slova
- 14,15-Epoxyeicosatrienoic acid analog, Myocardial ischemia/reperfusion injury, Renin−angiotensin system, Renovascular hypertension,
- MeSH
- ambulantní monitorování krevního tlaku metody MeSH
- aplikace orální MeSH
- časové faktory MeSH
- GSK3B MeSH
- infarkt myokardu metabolismus patologie prevence a kontrola MeSH
- kinasa 3 glykogensynthasy metabolismus MeSH
- krevní tlak účinky léků MeSH
- kyselina 8,11,14-eikosatrienová aplikace a dávkování analogy a deriváty MeSH
- kyseliny hydroxyeikosatetraenové metabolismus MeSH
- ledviny účinky léků metabolismus patologie MeSH
- modely nemocí na zvířatech MeSH
- myokard metabolismus patologie MeSH
- potkani Sprague-Dawley MeSH
- protoonkogenní proteiny c-akt metabolismus MeSH
- renin-angiotensin systém účinky léků MeSH
- renovaskulární hypertenze farmakoterapie metabolismus patofyziologie MeSH
- reperfuzní poškození myokardu metabolismus patologie prevence a kontrola MeSH
- signální transdukce účinky léků MeSH
- telemetrie MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
- Názvy látek
- 14,15-epoxy-5,8,11-eicosatrienoic acid MeSH Prohlížeč
- GSK3B MeSH
- kinasa 3 glykogensynthasy MeSH
- kyselina 8,11,14-eikosatrienová MeSH
- kyseliny hydroxyeikosatetraenové MeSH
- protoonkogenní proteiny c-akt MeSH
This study examined the effects of a novel orally active 14,15-epoxyeicosatrienoic acid analog (EET-A) on blood pressure (BP) and myocardial infarct size (IS) in two-kidney, one-clip (2K1C) Goldblatt hypertensive rats during sustained phase of hypertension. Between days 31 and 35 after clip placement the rats were treated with EET-A and BP was monitored by radiotelemetry; sham-operated normotensive rats were used as controls. Tissue concentrations of epoxyeicosatrienoic acids served as a marker of production of epoxygenase metabolites. The rats were subjected to acute myocardial ischemia/reperfusion (I/R) injury and IS was determined. We found that EET-A treatment did not lower BP in 2K1C rats and did not alter availability of biologically active epoxygenase metabolites in 2K1C or in sham-operated rats. The myocardial IS was significantly smaller in untreated 2K1C rats as compared with normotensive controls and EET-A reduced it in controls but not in 2K1C rats. Our findings suggest that during the phase of sustained hypertension 2K1C Goldblatt hypertensive rats exhibit increased cardiac tolerance to I/R injury as compared with normotensive controls, and that in this animal model of human renovascular hypertension short-term treatment with EET-A does not induce any antihypertensive and cardioprotective actions.
Department of Biochemistry University of Texas Southwestern Medical Center Dallas TX USA
Department of Cardiology Institute for Clinical and Experimental Medicine Prague Czech Republic
Department of Pharmacology and Toxicology Medical College of Wisconsin WI USA
Department of Pharmacology Kagawa University Kagawa Japan
Section of Nephrology Medical Polyclinic Department of Medicine University of Bonn Bonn Germany
Citace poskytuje Crossref.org
Sixty Years of Heart Research in the Institute of Physiology of the Czech Academy of Sciences
