Source:http://linkedlifedata.com/resource/pubmed/id/15734891
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2005-6-17
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| pubmed:abstractText |
To examine the mechanisms of changes in beta-adrenergic signal transduction in heart failing due to volume overload, we studied the status of beta-adrenoceptors (beta-ARs), G protein-coupled receptor kinase (GRK), and beta-arrestin in heart failure due to aortocaval shunt (AVS). Heart failure in rats was induced by creating AVS for 16 wk, and beta-AR binding, GRK activity, as well as their protein content, and mRNA levels were determined in both left and right ventricles. The density and protein content for beta1-ARs, unlike those for beta2-ARs, were increased in the failing hearts. Furthermore, protein contents for GRK isoforms and beta-arrestin-1 were decreased in membranous fractions and increased in cytosolic fractions from the failing hearts. On the other hand, steady-state mRNA levels for beta1-ARs and GRK2, as well as protein content for Gbetagamma-subunits, did not change in the failing heart. Basal cardiac function was depressed; however, both in vivo and ex vivo positive inotropic responses of the failing hearts to isoproterenol were augmented. Treatment of AVS animals with imidapril (1 mg.kg(-1).day(-1)) or losartan (20 mg.kg(-1).day(-1)) retarded the progression of heart failure; partially prevented changes in beta1-ARs, GRKs, and beta-arrestin-1 in the failing myocardium; and attenuated the increase in positive inotropic effect of isoproterenol. These results indicate that upregulation of beta1-ARs is associated with subcellular redistribution of GRKs and beta-arrestin-1 in the failing heart due to volume overload. Furthermore, attenuation of alterations in beta-adrenergic system by imidapril or losartan may be due to blockade of the renin-angiotensin system in the AVS model of heart failure.
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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/Arrestins,
http://linkedlifedata.com/resource/pubmed/chemical/Cardiotonic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP-Dependent Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/G-Protein-Coupled Receptor Kinase 5,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Protein beta Subunits,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Protein gamma Subunits,
http://linkedlifedata.com/resource/pubmed/chemical/Gprk5 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Isoproterenol,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta,
http://linkedlifedata.com/resource/pubmed/chemical/beta-Adrenergic Receptor Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/beta-arrestin
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
0363-6135
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
289
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
H151-9
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| pubmed:dateRevised |
2007-11-15
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| pubmed:meshHeading |
pubmed-meshheading:15734891-Animals,
pubmed-meshheading:15734891-Arrestins,
pubmed-meshheading:15734891-Blood Volume,
pubmed-meshheading:15734891-Cardiotonic Agents,
pubmed-meshheading:15734891-Cyclic AMP-Dependent Protein Kinases,
pubmed-meshheading:15734891-G-Protein-Coupled Receptor Kinase 5,
pubmed-meshheading:15734891-GTP-Binding Protein beta Subunits,
pubmed-meshheading:15734891-GTP-Binding Protein gamma Subunits,
pubmed-meshheading:15734891-Heart Failure,
pubmed-meshheading:15734891-Hemodynamics,
pubmed-meshheading:15734891-Isoproterenol,
pubmed-meshheading:15734891-Myocardium,
pubmed-meshheading:15734891-Protein-Serine-Threonine Kinases,
pubmed-meshheading:15734891-Rats,
pubmed-meshheading:15734891-Receptors, Adrenergic, beta,
pubmed-meshheading:15734891-Subcellular Fractions,
pubmed-meshheading:15734891-Tissue Distribution,
pubmed-meshheading:15734891-Up-Regulation,
pubmed-meshheading:15734891-beta-Adrenergic Receptor Kinases
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| pubmed:year |
2005
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| pubmed:articleTitle |
Upregulation of beta-adrenergic receptors in heart failure due to volume overload.
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| pubmed:affiliation |
Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, 351 Tache Ave., Winnipeg, MB R2H 2A6, Canada.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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