| pubmed-article:12631586 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12631586 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
| pubmed-article:12631586 | lifeskim:mentions | umls-concept:C1514559 | lld:lifeskim |
| pubmed-article:12631586 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:12631586 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:12631586 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:12631586 | pubmed:dateCreated | 2003-3-12 | lld:pubmed |
| pubmed-article:12631586 | pubmed:abstractText | The role of Galpha(i)-2 overexpression in desensitization of beta-adrenergic signaling in heart failure is controversial. An adenovirus-based approach was used to investigate whether overexpression of Galpha(i)-2 impairs beta-adrenergic stimulation of adenylyl cyclase (AC) activity and cAMP levels in neonatal rat cardiac myocytes (NRCM) and cell shortening of adult rat ventricular myocytes (ARVM). Infection of NRCM with Ad5Galpha(i)-2 increased Galpha(i)-2 by 50-600% in a virus dose-dependent manner. Overexpression was paralleled by suppression of GTP- and isoprenaline-stimulated AC by 10-72% (P<0.001) in a PTX-sensitive manner. Isoprenaline-stimulated shortening of Ad5Galpha(i)-2-infected ARVM was attenuated by 34% (P<0.01). Ad5Galpha(i)-2/GFP (Galpha(i)-2, green fluorescent protein; bicistronic) was constructed to monitor transfection homogeneity and target Galpha(i)-2 overexpression to levels found in heart failure. At Galpha(i)-2 levels of 93% above control, isoprenaline-stimulated AC activity and cAMP levels were reduced by 17% and 40% (P<0.02), respectively. Beta1- and beta2-adrenergic stimulation was reduced similarly. Our results suggest that (a) the Galpha(i)-2 system exhibits tonic inhibition of stimulated AC in cardiac myocytes, (b) Galpha(i)-2-mediated inhibition is concentration-dependent and occurs at Galpha(i)-2 levels seen in heart failure, and (c) Galpha(i)-2-mediated inhibition affects both beta1- and beta2-adrenergic stimulation of AC. The data argue for an important, independent role of the Galpha(i)-2 increase in heart failure. | lld:pubmed |
| pubmed-article:12631586 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12631586 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12631586 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12631586 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12631586 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12631586 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12631586 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12631586 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12631586 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12631586 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12631586 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12631586 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12631586 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12631586 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:12631586 | pubmed:issn | 1530-6860 | lld:pubmed |
| pubmed-article:12631586 | pubmed:author | pubmed-author:KochWalter... | lld:pubmed |
| pubmed-article:12631586 | pubmed:author | pubmed-author:EschenhagenTh... | lld:pubmed |
| pubmed-article:12631586 | pubmed:author | pubmed-author:WeilJoachimJ | lld:pubmed |
| pubmed-article:12631586 | pubmed:author | pubmed-author:RauThomasT | lld:pubmed |
| pubmed-article:12631586 | pubmed:author | pubmed-author:DaviaKerryK | lld:pubmed |
| pubmed-article:12631586 | pubmed:author | pubmed-author:NoseMonikaM | lld:pubmed |
| pubmed-article:12631586 | pubmed:author | pubmed-author:PeppelKarsten... | lld:pubmed |
| pubmed-article:12631586 | pubmed:author | pubmed-author:RemmersUteU | lld:pubmed |
| pubmed-article:12631586 | pubmed:author | pubmed-author:WeissmüllerAs... | lld:pubmed |
| pubmed-article:12631586 | pubmed:author | pubmed-author:HardingSianS | lld:pubmed |
| pubmed-article:12631586 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:12631586 | pubmed:volume | 17 | lld:pubmed |
| pubmed-article:12631586 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12631586 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12631586 | pubmed:pagination | 523-5 | lld:pubmed |
| pubmed-article:12631586 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:12631586 | pubmed:meshHeading | pubmed-meshheading:12631586... | lld:pubmed |
| pubmed-article:12631586 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12631586 | pubmed:articleTitle | Overexpression of wild-type Galpha(i)-2 suppresses beta-adrenergic signaling in cardiac myocytes. | lld:pubmed |
| pubmed-article:12631586 | pubmed:affiliation | Institute of Pharmacology and Toxicology, Friedrich Alexander University Erlangen, Germany. | lld:pubmed |
| pubmed-article:12631586 | pubmed:publicationType | Journal Article | lld:pubmed |
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