rdf:type |
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lifeskim:mentions |
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pubmed:issue |
25
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pubmed:dateCreated |
2001-12-18
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pubmed:abstractText |
The major source of nitric oxide (NO) in the heart is the constitutive form of NO synthases (eNOS, NOS III) that is expressed in vascular endothelium and cardiac myocytes. NO mediates endothelium-dependent vasodilation and may modulate cardiac function. We examined the role of NO in hearts from transgenic (TG) mice overexpressing eNOS exclusively in cardiac myocytes.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholine,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/NG-Nitroarginine Methyl Ester,
http://linkedlifedata.com/resource/pubmed/chemical/NOS3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type III,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Nos3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Vasoconstrictor Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Vasodilator Agents
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1524-4539
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
18
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pubmed:volume |
104
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3097-102
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:11748107-Acetylcholine,
pubmed-meshheading:11748107-Animals,
pubmed-meshheading:11748107-Calcium,
pubmed-meshheading:11748107-Dose-Response Relationship, Drug,
pubmed-meshheading:11748107-Enzyme Inhibitors,
pubmed-meshheading:11748107-Female,
pubmed-meshheading:11748107-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:11748107-Genotype,
pubmed-meshheading:11748107-Heart Rate,
pubmed-meshheading:11748107-Heart Ventricles,
pubmed-meshheading:11748107-Humans,
pubmed-meshheading:11748107-Male,
pubmed-meshheading:11748107-Mice,
pubmed-meshheading:11748107-Mice, Inbred C57BL,
pubmed-meshheading:11748107-Mice, Inbred CBA,
pubmed-meshheading:11748107-Mice, Transgenic,
pubmed-meshheading:11748107-Myocardial Contraction,
pubmed-meshheading:11748107-Myocardium,
pubmed-meshheading:11748107-NG-Nitroarginine Methyl Ester,
pubmed-meshheading:11748107-Nitric Oxide Synthase,
pubmed-meshheading:11748107-Nitric Oxide Synthase Type II,
pubmed-meshheading:11748107-Nitric Oxide Synthase Type III,
pubmed-meshheading:11748107-Norepinephrine,
pubmed-meshheading:11748107-Vasoconstrictor Agents,
pubmed-meshheading:11748107-Vasodilator Agents,
pubmed-meshheading:11748107-Ventricular Function
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pubmed:year |
2001
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pubmed:articleTitle |
Myocardial contractile function and heart rate in mice with myocyte-specific overexpression of endothelial nitric oxide synthase.
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pubmed:affiliation |
Institut für Pharmakologie und Toxikologie, the Institut für Molekularbiologie, Biochemie und Mikrobiologie, Karl-Franzens-Universität Graz, Graz, Austria. friedrich.brunner@kfunigraz.ac.at
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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