| pubmed-article:19887855 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19887855 | lifeskim:mentions | umls-concept:C0021289 | lld:lifeskim |
| pubmed-article:19887855 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
| pubmed-article:19887855 | lifeskim:mentions | umls-concept:C0017710 | lld:lifeskim |
| pubmed-article:19887855 | lifeskim:mentions | umls-concept:C0034787 | lld:lifeskim |
| pubmed-article:19887855 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:19887855 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:19887855 | pubmed:dateCreated | 2010-3-24 | lld:pubmed |
| pubmed-article:19887855 | pubmed:abstractText | Perinatal glucocorticoid treatment is associated with hypertrophic cardiomyopathy, but the cellular mechanism is controversial. An underlying interaction between glucocorticoids and the renin-angiotensin system may be important, but whether glucocorticoids modulate angiotensin II (AngII)-dependent cardiomyocyte growth responses in the neonate has not been investigated. Objectives: The major aim of this investigation was to determine whether glucocorticoids modulate the neonatal cardiomyocyte growth response to AngII. In particular we sought evidence to determine whether angiotensin II type 2 (AT(2)) receptor co-expression with angiotensin II type 1 (AT(1)) receptor is of specific importance in this modulatory function. | lld:pubmed |
| pubmed-article:19887855 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19887855 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19887855 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19887855 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19887855 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19887855 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19887855 | pubmed:issn | 1661-7819 | lld:pubmed |
| pubmed-article:19887855 | pubmed:author | pubmed-author:ThomasWalter... | lld:pubmed |
| pubmed-article:19887855 | pubmed:author | pubmed-author:WiddopRobert... | lld:pubmed |
| pubmed-article:19887855 | pubmed:author | pubmed-author:DelbridgeLea... | lld:pubmed |
| pubmed-article:19887855 | pubmed:author | pubmed-author:PorrelloEnzo... | lld:pubmed |
| pubmed-article:19887855 | pubmed:author | pubmed-author:MeekerWilliam... | lld:pubmed |
| pubmed-article:19887855 | pubmed:copyrightInfo | Copyright 2009 S. Karger AG, Basel. | lld:pubmed |
| pubmed-article:19887855 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19887855 | pubmed:volume | 97 | lld:pubmed |
| pubmed-article:19887855 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19887855 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19887855 | pubmed:pagination | 257-65 | lld:pubmed |
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| pubmed-article:19887855 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:19887855 | pubmed:articleTitle | Glucocorticoids suppress growth in neonatal cardiomyocytes co-expressing AT(2) and AT(1) angiotensin receptors. | lld:pubmed |
| pubmed-article:19887855 | pubmed:affiliation | Department of Physiology, The University of Melbourne, Parkville,Vic. 3010, Australia. | lld:pubmed |
| pubmed-article:19887855 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19887855 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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