| pubmed-article:17322894 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17322894 | lifeskim:mentions | umls-concept:C0018801 | lld:lifeskim |
| pubmed-article:17322894 | lifeskim:mentions | umls-concept:C0521428 | lld:lifeskim |
| pubmed-article:17322894 | lifeskim:mentions | umls-concept:C0041904 | lld:lifeskim |
| pubmed-article:17322894 | lifeskim:mentions | umls-concept:C1366490 | lld:lifeskim |
| pubmed-article:17322894 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
| pubmed-article:17322894 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:17322894 | pubmed:dateCreated | 2007-3-7 | lld:pubmed |
| pubmed-article:17322894 | pubmed:abstractText | Cardiac overstimulation by the sympathetic nervous system (SNS) is a salient characteristic of heart failure, reflected by elevated circulating levels of catecholamines. The success of beta-adrenergic receptor (betaAR) antagonists in heart failure argues for SNS hyperactivity being pathogenic; however, sympatholytic agents targeting alpha2AR-mediated catecholamine inhibition have been unsuccessful. By investigating adrenal adrenergic receptor signaling in heart failure models, we found molecular mechanisms to explain the failure of sympatholytic agents and discovered a new strategy to lower SNS activity. During heart failure, there is substantial alpha2AR dysregulation in the adrenal gland, triggered by increased expression and activity of G protein-coupled receptor kinase 2 (GRK2). Adrenal gland-specific GRK2 inhibition reversed alpha2AR dysregulation in heart failure, resulting in lowered plasma catecholamine levels, improved cardiac betaAR signaling and function, and increased sympatholytic efficacy of a alpha2AR agonist. This is the first demonstration, to our knowledge, of a molecular mechanism for SNS hyperactivity in heart failure, and our study identifies adrenal GRK2 activity as a new sympatholytic target. | lld:pubmed |
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| pubmed-article:17322894 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:17322894 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17322894 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17322894 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:17322894 | pubmed:issn | 1078-8956 | lld:pubmed |
| pubmed-article:17322894 | pubmed:author | pubmed-author:KochWalter... | lld:pubmed |
| pubmed-article:17322894 | pubmed:author | pubmed-author:EckhartAndrea... | lld:pubmed |
| pubmed-article:17322894 | pubmed:author | pubmed-author:FunakoshiHaji... | lld:pubmed |
| pubmed-article:17322894 | pubmed:author | pubmed-author:Lymperopoulos... | lld:pubmed |
| pubmed-article:17322894 | pubmed:author | pubmed-author:RengoGiuseppe... | lld:pubmed |
| pubmed-article:17322894 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17322894 | pubmed:volume | 13 | lld:pubmed |
| pubmed-article:17322894 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17322894 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17322894 | pubmed:pagination | 315-23 | lld:pubmed |
| pubmed-article:17322894 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:17322894 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17322894 | pubmed:articleTitle | Adrenal GRK2 upregulation mediates sympathetic overdrive in heart failure. | lld:pubmed |
| pubmed-article:17322894 | pubmed:affiliation | Center for Translational Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA. | lld:pubmed |
| pubmed-article:17322894 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17322894 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17322894 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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