Source:http://linkedlifedata.com/resource/pubmed/id/10216249
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1999-6-10
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pubmed:abstractText |
The present study investigated the involvement of endothelial nitric oxide in relaxation induced by purified green tea (-)epicatechin in rat isolated mesenteric arteries. (-)Epicatechin caused both endothelium-dependent and -independent relaxation. NG-Nitro-L-arginine methyl ester (L-NAME, 100 microM) and methylene blue (10 microM) significantly attenuated (-)epicatechin-induced relaxation in endothelium-intact tissues. L-Arginine (1 mM) partially antagonized the effect of L-NAME. (-)Epicatechin-induced relaxation was inhibited by Rp-guanosine 3',5'-cyclic monophosphothioate triethylamine. In contrast, indomethacin and glibenclamide had no effect. (-)Epicatechin (100 microM) significantly increased the tissue content of cyclic GMP and NG-nitro-L-arginine (100 microM) or removal of the endothelium abolished this increase. (-)Epicatechin (100 microM) induced an increase in intracellular Ca2+ levels in cultured human umbilical vein endothelial cells. Iberiotoxin at 100 nM attenuated (-)epicatechin-induced relaxation in endothelium-intact arteries and this effect was absent in the presence of 100 microM L-NAME. In summary, (-)epicatechin-induced endothelium-dependent relaxation is primarily mediated by nitric oxide and partially through nitric oxide-dependent activation of iberiotoxin-sensitive K+ channels. In addition, there may be a causal link between increased Ca2+ levels and nitric oxide release in response to (-)epicatechin.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Catechin,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic GMP,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Phenylephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Tea
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0006-3002
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
19
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pubmed:volume |
1427
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
322-8
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:10216249-Animals,
pubmed-meshheading:10216249-Calcium Channels,
pubmed-meshheading:10216249-Catechin,
pubmed-meshheading:10216249-Cyclic GMP,
pubmed-meshheading:10216249-Dose-Response Relationship, Drug,
pubmed-meshheading:10216249-Endothelium, Vascular,
pubmed-meshheading:10216249-Male,
pubmed-meshheading:10216249-Mesenteric Arteries,
pubmed-meshheading:10216249-Muscle, Smooth, Vascular,
pubmed-meshheading:10216249-Nitric Oxide,
pubmed-meshheading:10216249-Phenylephrine,
pubmed-meshheading:10216249-Rats,
pubmed-meshheading:10216249-Rats, Sprague-Dawley,
pubmed-meshheading:10216249-Tea,
pubmed-meshheading:10216249-Vasodilation
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pubmed:year |
1999
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pubmed:articleTitle |
Involvement of endothelium/nitric oxide in vasorelaxation induced by purified green tea (-)epicatechin.
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pubmed:affiliation |
Department of Physiology, Chinese University of Hong Kong, Faculty of Medicine, Shatin, Hong Kong. yu-huang@cuhk.edu.hk
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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