pubmed-article:10953023 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10953023 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
pubmed-article:10953023 | lifeskim:mentions | umls-concept:C0014257 | lld:lifeskim |
pubmed-article:10953023 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
pubmed-article:10953023 | lifeskim:mentions | umls-concept:C0547040 | lld:lifeskim |
pubmed-article:10953023 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
pubmed-article:10953023 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:10953023 | pubmed:dateCreated | 2000-9-18 | lld:pubmed |
pubmed-article:10953023 | pubmed:abstractText | Homocysteine is a risk factor for the development of atherosclerosis and its thrombotic complications. We have employed an animal model to explore the hypothesis that an increase in reactive oxygen species and a subsequent loss of nitric oxide bioactivity contribute to endothelial dysfunction in mild hyperhomocysteinemia. We examined endothelial function and in vivo oxidant burden in mice heterozygous for a deletion in the cystathionine beta-synthase (CBS) gene, by studying isolated, precontracted aortic rings and mesenteric arterioles in situ. CBS(-/+) mice demonstrated impaired acetylcholine-induced aortic relaxation and a paradoxical vasoconstriction of mesenteric microvessels in response to superfusion of methacholine and bradykinin. Cyclic GMP accumulation following acetylcholine treatment was also impaired in isolated aortic segments from CBS(-/+) mice, but aortic relaxation and mesenteric arteriolar dilation in response to sodium nitroprusside were similar to wild-type. Plasma levels of 8-epi-PGF(2alpha) (8-IP) were somewhat increased in CBS(-/+) mice, but liver levels of 8-IP and phospholipid hydroperoxides, another marker of oxidative stress, were normal. Aortic tissue from CBS(-/+) mice also demonstrated greater superoxide production and greater immunostaining for 3-nitrotyrosine, particularly on the endothelial surface. Importantly, endothelial dysfunction appears early in CBS(-/+) mice in the absence of structural arterial abnormalities. Hence, mild hyperhomocysteinemia due to reduced CBS expression impairs endothelium-dependent vasodilation, likely due to impaired nitric oxide bioactivity, and increased oxidative stress apparently contributes to inactivating nitric oxide in chronic, mild hyperhomocysteinemia. | lld:pubmed |
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pubmed-article:10953023 | pubmed:language | eng | lld:pubmed |
pubmed-article:10953023 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10953023 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:10953023 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10953023 | pubmed:month | Aug | lld:pubmed |
pubmed-article:10953023 | pubmed:issn | 0021-9738 | lld:pubmed |
pubmed-article:10953023 | pubmed:author | pubmed-author:StarkRR | lld:pubmed |
pubmed-article:10953023 | pubmed:author | pubmed-author:CohenRR | lld:pubmed |
pubmed-article:10953023 | pubmed:author | pubmed-author:LoscalzoJJ | lld:pubmed |
pubmed-article:10953023 | pubmed:author | pubmed-author:CauDD | lld:pubmed |
pubmed-article:10953023 | pubmed:author | pubmed-author:Goldschmidt-C... | lld:pubmed |
pubmed-article:10953023 | pubmed:author | pubmed-author:FarberH WHW | lld:pubmed |
pubmed-article:10953023 | pubmed:author | pubmed-author:RuddM AMA | lld:pubmed |
pubmed-article:10953023 | pubmed:author | pubmed-author:HeydrickSS | lld:pubmed |
pubmed-article:10953023 | pubmed:author | pubmed-author:LeopoldJ AJA | lld:pubmed |
pubmed-article:10953023 | pubmed:author | pubmed-author:MoldovanN INI | lld:pubmed |
pubmed-article:10953023 | pubmed:author | pubmed-author:EberhardtR... | lld:pubmed |
pubmed-article:10953023 | pubmed:author | pubmed-author:TrollietMM | lld:pubmed |
pubmed-article:10953023 | pubmed:author | pubmed-author:YaghoubiMM | lld:pubmed |
pubmed-article:10953023 | pubmed:author | pubmed-author:KlingsE SES | lld:pubmed |
pubmed-article:10953023 | pubmed:author | pubmed-author:ForgioneM AMA | lld:pubmed |
pubmed-article:10953023 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10953023 | pubmed:volume | 106 | lld:pubmed |
pubmed-article:10953023 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10953023 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10953023 | pubmed:pagination | 483-91 | lld:pubmed |
pubmed-article:10953023 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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