pubmed-article:12384455 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12384455 | lifeskim:mentions | umls-concept:C0684336 | lld:lifeskim |
pubmed-article:12384455 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:12384455 | lifeskim:mentions | umls-concept:C0205042 | lld:lifeskim |
pubmed-article:12384455 | lifeskim:mentions | umls-concept:C0042401 | lld:lifeskim |
pubmed-article:12384455 | lifeskim:mentions | umls-concept:C0007745 | lld:lifeskim |
pubmed-article:12384455 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:12384455 | pubmed:dateCreated | 2002-10-17 | lld:pubmed |
pubmed-article:12384455 | pubmed:abstractText | The present study tested the hypothesis that ceramide, a sphingomylinase metabolite, serves as an second messenger for tumor necrosis factor-alpha (TNF-alpha) to stimulate superoxide production, thereby decreasing endothelium-dependent vasorelaxation in coronary arteries. In isolated bovine small coronary arteries, TNF-alpha (1 ng/ml) markedly attenuated vasodilator responses to bradykinin and A-23187. In the presence of N(G)-nitro-L-arginine methyl ester, TNF-alpha produced no further inhibition on the vasorelaxation induced by these vasodilators. With the use of 4,5-diaminofluorescein diacetate fluorescence imaging analysis, bradykinin was found to increase nitric oxide (NO) concentrations in the endothelium of isolated bovine small coronary arteries, which was inhibited by TNF-alpha. Pretreatment of the arteries with desipramine (10 microM), an inhibitor of acidic sphingomyelinase, tiron (1 mM), a superoxide scavenger, and polyethylene glycol-superoxide dismutase (100 U/ml) largely restored the inhibitory effect of TNF-alpha on bradykinin- and A-23187-induced vasorelaxation. In addition, TNF-alpha activated acidic sphingomyelinase and increased ceramide levels in coronary endothelial cells. We conclude that TNF-alpha inhibits NO-mediated endothelium-dependent vasorelaxation in small coronary arteries via sphingomyelinase activation and consequent superoxide production in endothelial cells. | lld:pubmed |
pubmed-article:12384455 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12384455 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12384455 | pubmed:language | eng | lld:pubmed |
pubmed-article:12384455 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12384455 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:12384455 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12384455 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12384455 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12384455 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12384455 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12384455 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12384455 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12384455 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12384455 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12384455 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12384455 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12384455 | pubmed:month | Nov | lld:pubmed |
pubmed-article:12384455 | pubmed:issn | 0363-6135 | lld:pubmed |
pubmed-article:12384455 | pubmed:author | pubmed-author:ZouAi-PingAP | lld:pubmed |
pubmed-article:12384455 | pubmed:author | pubmed-author:LiPin-LanPL | lld:pubmed |
pubmed-article:12384455 | pubmed:author | pubmed-author:ZhangDavid... | lld:pubmed |
pubmed-article:12384455 | pubmed:author | pubmed-author:YiFu-XianFX | lld:pubmed |
pubmed-article:12384455 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12384455 | pubmed:volume | 283 | lld:pubmed |
pubmed-article:12384455 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12384455 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12384455 | pubmed:pagination | H1785-94 | lld:pubmed |
pubmed-article:12384455 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:12384455 | pubmed:meshHeading | pubmed-meshheading:12384455... | lld:pubmed |
pubmed-article:12384455 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:12384455 | pubmed:articleTitle | Role of ceramide in TNF-alpha-induced impairment of endothelium-dependent vasorelaxation in coronary arteries. | lld:pubmed |
pubmed-article:12384455 | pubmed:affiliation | Department of Pharmacology and Toxicology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA. | lld:pubmed |
pubmed-article:12384455 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12384455 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:12384455 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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