Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:18375719rdf:typepubmed:Citationlld:pubmed
pubmed-article:18375719lifeskim:mentionsumls-concept:C0035820lld:lifeskim
pubmed-article:18375719lifeskim:mentionsumls-concept:C0034721lld:lifeskim
pubmed-article:18375719lifeskim:mentionsumls-concept:C0034693lld:lifeskim
pubmed-article:18375719lifeskim:mentionsumls-concept:C0025465lld:lifeskim
pubmed-article:18375719lifeskim:mentionsumls-concept:C0010762lld:lifeskim
pubmed-article:18375719lifeskim:mentionsumls-concept:C0032214lld:lifeskim
pubmed-article:18375719lifeskim:mentionsumls-concept:C0035028lld:lifeskim
pubmed-article:18375719lifeskim:mentionsumls-concept:C0870883lld:lifeskim
pubmed-article:18375719lifeskim:mentionsumls-concept:C0596235lld:lifeskim
pubmed-article:18375719lifeskim:mentionsumls-concept:C0205263lld:lifeskim
pubmed-article:18375719lifeskim:mentionsumls-concept:C0299477lld:lifeskim
pubmed-article:18375719pubmed:issue5lld:pubmed
pubmed-article:18375719pubmed:dateCreated2008-5-7lld:pubmed
pubmed-article:18375719pubmed:abstractTextThe perivascular sensory nerve (PvN) Ca(2+)-sensing receptor (CaR) is implicated in Ca(2+)-induced relaxation of isolated, phenylephrine (PE)-contracted mesenteric arteries, which involves the vascular endogenous cannabinoid system. We determined the effect of inhibition of diacylglycerol (DAG) lipase (DAGL), phospholipase A(2) (PLA(2)), and cytochrome P-450 (CYP) on Ca(2+)-induced relaxation of PE-contracted rat mesenteric arteries. Our findings indicate that Ca(2+)-induced vasorelaxation is not dependent on the endothelium. The DAGL inhibitor RHC 802675 (1 microM) and the CYP and PLA(2) inhibitors quinacrine (5 microM) (EC(50): RHC 802675 2.8 +/- 0.4 mM vs. control 1.4 +/- 0.3 mM; quinacrine 4.8 +/- 0.4 mM vs. control 2.0 +/- 0.3 mM; n = 5) and arachidonyltrifluoromethyl ketone (AACOCF(3), 1 microM) reduced Ca(2+)-induced relaxation of mesenteric arteries. Synthetic 2-arachidonoylglycerol (2-AG) and glycerated epoxyeicosatrienoic acids (GEETs) induced concentration-dependent relaxation of isolated arteries. 2-AG relaxations were blocked by iberiotoxin (IBTX) (EC(50): control 0.96 +/- 0.14 nM, IBTX 1.3 +/- 0.5 microM) and miconazole (48 +/- 3%), and 11,12-GEET responses were blocked by IBTX (EC(50): control 55 +/- 9 nM, IBTX 690 +/- 96 nM) and SR-141716A. The data suggest that activation of the CaR in the PvN network by Ca(2+) leads to synthesis and/or release of metabolites of the CYP epoxygenase pathway and metabolism of DAG to 2-AG and subsequently to GEETs. The findings indicate a role for 2-AG and its metabolites in Ca(2+)-induced relaxation of resistance arteries; therefore this receptor may be a potential target for the development of new vasodilator compounds for antihypertensive therapy.lld:pubmed
pubmed-article:18375719pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:languageenglld:pubmed
pubmed-article:18375719pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:citationSubsetIMlld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18375719pubmed:statusMEDLINElld:pubmed
pubmed-article:18375719pubmed:monthMaylld:pubmed
pubmed-article:18375719pubmed:issn0363-6135lld:pubmed
pubmed-article:18375719pubmed:authorpubmed-author:BukoskiRichar...lld:pubmed
pubmed-article:18375719pubmed:authorpubmed-author:DizDebra IDIlld:pubmed
pubmed-article:18375719pubmed:authorpubmed-author:AwumeyEmmanue...lld:pubmed
pubmed-article:18375719pubmed:authorpubmed-author:HillSylvie...lld:pubmed
pubmed-article:18375719pubmed:issnTypePrintlld:pubmed
pubmed-article:18375719pubmed:volume294lld:pubmed
pubmed-article:18375719pubmed:ownerNLMlld:pubmed
pubmed-article:18375719pubmed:authorsCompleteYlld:pubmed
pubmed-article:18375719pubmed:paginationH2363-70lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:meshHeadingpubmed-meshheading:18375719...lld:pubmed
pubmed-article:18375719pubmed:year2008lld:pubmed
pubmed-article:18375719pubmed:articleTitleCytochrome P-450 metabolites of 2-arachidonoylglycerol play a role in Ca2+-induced relaxation of rat mesenteric arteries.lld:pubmed
pubmed-article:18375719pubmed:affiliationCardiovascular Disease Research Program, Julius L. Chambers Biomedical/Biotechnology Research Institute, North Carolina Central University, 700 George Street, Durham, NC 27707, USA. eawumey@nccu.edulld:pubmed
pubmed-article:18375719pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:18375719pubmed:publicationTypeResearch Support, N.I.H., Extramurallld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:18375719lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:18375719lld:pubmed