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rdf:type |
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lifeskim:mentions |
umls-concept:C0014257,
umls-concept:C0031715,
umls-concept:C0087111,
umls-concept:C0248719,
umls-concept:C0277785,
umls-concept:C0597357,
umls-concept:C0907532,
umls-concept:C1280500,
umls-concept:C1314939,
umls-concept:C1412113,
umls-concept:C1704410
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pubmed:issue |
10
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pubmed:dateCreated |
2011-9-15
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pubmed:abstractText |
Continuous administration of nitroglycerin (GTN) causes tolerance and endothelial dysfunction by inducing reactive oxygen species (ROS) production from various enzymatic sources, such as mitochondria, NADPH oxidase, and an uncoupled endothelial nitric oxide synthase (eNOS). In the present study, we tested the effects of type 1 angiotensin (AT(1))-receptor blockade with telmisartan on GTN-induced endothelial dysfunction in particular on eNOS phosphorylation and S-glutathionylation sites and the eNOS cofactor synthesizing enzyme GTP-cyclohydrolase I.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Aldehyde Dehydrogenase,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II Type 1 Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Benzimidazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Benzoates,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/GTP Cyclohydrolase,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type III,
http://linkedlifedata.com/resource/pubmed/chemical/Nitroglycerin,
http://linkedlifedata.com/resource/pubmed/chemical/Nos3 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrahydrofolate Dehydrogenase,
http://linkedlifedata.com/resource/pubmed/chemical/Vasodilator Agents,
http://linkedlifedata.com/resource/pubmed/chemical/telmisartan
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1524-4636
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pubmed:author |
pubmed-author:DaiberAndreasA,
pubmed-author:GoriTommasoT,
pubmed-author:HausdingMichaelM,
pubmed-author:HeerenTjeboT,
pubmed-author:KnorrMaikeM,
pubmed-author:Kröller-SchuhmacherSwenjaS,
pubmed-author:MünzelThomasT,
pubmed-author:OelzeMatthiasM,
pubmed-author:ScholzAlexanderA,
pubmed-author:SchulzEberhardE,
pubmed-author:StevenSebastianS,
pubmed-author:WenzelPhilipP
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pubmed:issnType |
Electronic
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pubmed:volume |
31
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2223-31
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pubmed:meshHeading |
pubmed-meshheading:21757654-Aldehyde Dehydrogenase,
pubmed-meshheading:21757654-Angiotensin II Type 1 Receptor Blockers,
pubmed-meshheading:21757654-Animals,
pubmed-meshheading:21757654-Benzimidazoles,
pubmed-meshheading:21757654-Benzoates,
pubmed-meshheading:21757654-Cell Line,
pubmed-meshheading:21757654-Dose-Response Relationship, Drug,
pubmed-meshheading:21757654-Drug Tolerance,
pubmed-meshheading:21757654-Endothelial Cells,
pubmed-meshheading:21757654-Endothelium, Vascular,
pubmed-meshheading:21757654-Enzyme Inhibitors,
pubmed-meshheading:21757654-GTP Cyclohydrolase,
pubmed-meshheading:21757654-Glutathione,
pubmed-meshheading:21757654-Humans,
pubmed-meshheading:21757654-Male,
pubmed-meshheading:21757654-Mitochondria,
pubmed-meshheading:21757654-Nitric Oxide Synthase Type III,
pubmed-meshheading:21757654-Nitroglycerin,
pubmed-meshheading:21757654-Oxidative Stress,
pubmed-meshheading:21757654-Phosphorylation,
pubmed-meshheading:21757654-Protein Processing, Post-Translational,
pubmed-meshheading:21757654-Rats,
pubmed-meshheading:21757654-Rats, Wistar,
pubmed-meshheading:21757654-Reactive Oxygen Species,
pubmed-meshheading:21757654-Tetrahydrofolate Dehydrogenase,
pubmed-meshheading:21757654-Vasodilation,
pubmed-meshheading:21757654-Vasodilator Agents
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pubmed:year |
2011
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pubmed:articleTitle |
Nitroglycerin-induced endothelial dysfunction and tolerance involve adverse phosphorylation and S-Glutathionylation of endothelial nitric oxide synthase: beneficial effects of therapy with the AT1 receptor blocker telmisartan.
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pubmed:affiliation |
Second Medical Clinic, Department of Cardiology, Medical Center of Johannes Gutenberg University, Mainz, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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