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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
13
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pubmed:dateCreated |
2003-9-30
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pubmed:abstractText |
Myocardial contractile response to beta1- and beta2-adrenergic receptor (AR) stimulation is severely impaired in chronic heart failure, in which G(i) signaling and the ratio of beta2/beta1 are often increased. Because beta2-AR but not beta1-AR couples to G(s) and G(i) with the G(i) coupling negating the G(s)-mediated contractile response, we determined whether the heart failure-associated augmentation of G(i) signaling contributes differentially to the defects of these beta-AR subtypes and, if so, whether inhibition of G(i) or selective activation of beta2-AR/G(s) by ligands restores beta2-AR contractile response in the failing heart.
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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/Adrenergic beta-1 Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-2 Receptor Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Cardiotonic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Fenoterol,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Protein alpha...,
http://linkedlifedata.com/resource/pubmed/chemical/Heterotrimeric GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/Pertussis Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta-1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta-2
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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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 |
30
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pubmed:volume |
108
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1633-9
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:12975249-Adrenergic beta-1 Receptor Antagonists,
pubmed-meshheading:12975249-Adrenergic beta-2 Receptor Agonists,
pubmed-meshheading:12975249-Adrenergic beta-Agonists,
pubmed-meshheading:12975249-Animals,
pubmed-meshheading:12975249-Cardiac Output, Low,
pubmed-meshheading:12975249-Cardiotonic Agents,
pubmed-meshheading:12975249-Cells, Cultured,
pubmed-meshheading:12975249-Chronic Disease,
pubmed-meshheading:12975249-Fenoterol,
pubmed-meshheading:12975249-GTP-Binding Protein alpha Subunits, Gi-Go,
pubmed-meshheading:12975249-Heterotrimeric GTP-Binding Proteins,
pubmed-meshheading:12975249-Ligands,
pubmed-meshheading:12975249-Myocardial Contraction,
pubmed-meshheading:12975249-Myocardium,
pubmed-meshheading:12975249-Myocytes, Cardiac,
pubmed-meshheading:12975249-Pertussis Toxin,
pubmed-meshheading:12975249-Rats,
pubmed-meshheading:12975249-Rats, Inbred SHR,
pubmed-meshheading:12975249-Rats, Inbred WKY,
pubmed-meshheading:12975249-Receptors, Adrenergic, beta-1,
pubmed-meshheading:12975249-Receptors, Adrenergic, beta-2,
pubmed-meshheading:12975249-Signal Transduction
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pubmed:year |
2003
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pubmed:articleTitle |
Enhanced G(i) signaling selectively negates beta2-adrenergic receptor (AR)--but not beta1-AR-mediated positive inotropic effect in myocytes from failing rat hearts.
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pubmed:affiliation |
the Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Md 21224, USA. xiaor@grc.nia.nih.gov
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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