| pubmed-article:12030381 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12030381 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
| pubmed-article:12030381 | lifeskim:mentions | umls-concept:C0595934 | lld:lifeskim |
| pubmed-article:12030381 | lifeskim:mentions | umls-concept:C0678226 | lld:lifeskim |
| pubmed-article:12030381 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:12030381 | lifeskim:mentions | umls-concept:C1515926 | lld:lifeskim |
| pubmed-article:12030381 | pubmed:issue | 1-2 | lld:pubmed |
| pubmed-article:12030381 | pubmed:dateCreated | 2002-5-27 | lld:pubmed |
| pubmed-article:12030381 | pubmed:abstractText | In order to understand the modification of beta-adrenoceptor linked signal transduction by changes in the intracellular Ca2+, we examined the status of beta-adrenoceptors (beta-ARs), G-proteins and adenylyl cyclase (AC) in Ca2+-deficiency and Ca2+-overload by perfusing the isolated rat heart with Ca2+-free medium for 5 min and Ca2+-containing medium for 5 min following Ca2+-free perfusion, respectively. Ca2+-depletion caused not only an increase in basal, isoproterenol-, Gpp(NH)p-, NaF- and forskolin-stimulated AC activities but also produced an increase in the beta1-AR affinity and density as well as up-regulation of G(s)-protein function and uncoupling of G(i)-protein to AC. Ca2+-repletion for 5 min following 5 min Ca2+-free perfusion reversed the increased AC activities to varying degrees. The beta1-AR affinity was further increased upon Ca2+-repletion whereas its density was decreased. Ca2+-repletion also decreased protein content for AC and beta-AR kinase but augmented the changes in G(s)- and G(i)-protein functions. Although low Na+ medium perfusion during Ca2+-depletion prevented the changes in G-proteins during both Ca2+-depletion and Ca2+-repletion periods, the increased beta1-AR affinity and density as well as changes in AC activities due to Ca2+-depletion were not affected while alterations due to Ca2+-repletion were fully prevented. These results suggest that changes in Ca2+-homeostasis may represent a mechanism for alterations in the beta-adrenergic signal transduction pathway in the heart under pathological conditions. | lld:pubmed |
| pubmed-article:12030381 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12030381 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12030381 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12030381 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12030381 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12030381 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12030381 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12030381 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12030381 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12030381 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12030381 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:12030381 | pubmed:issn | 0300-8177 | lld:pubmed |
| pubmed-article:12030381 | pubmed:author | pubmed-author:DhallaNaranja... | lld:pubmed |
| pubmed-article:12030381 | pubmed:author | pubmed-author:TakedaSatoshi... | lld:pubmed |
| pubmed-article:12030381 | pubmed:author | pubmed-author:WangXiX | lld:pubmed |
| pubmed-article:12030381 | pubmed:author | pubmed-author:WangJingweiJ | lld:pubmed |
| pubmed-article:12030381 | pubmed:author | pubmed-author:ElimbanVijaya... | lld:pubmed |
| pubmed-article:12030381 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12030381 | pubmed:volume | 232 | lld:pubmed |
| pubmed-article:12030381 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12030381 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12030381 | pubmed:pagination | 63-73 | lld:pubmed |
| pubmed-article:12030381 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:12030381 | pubmed:meshHeading | pubmed-meshheading:12030381... | lld:pubmed |
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| pubmed-article:12030381 | pubmed:meshHeading | pubmed-meshheading:12030381... | lld:pubmed |
| pubmed-article:12030381 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12030381 | pubmed:articleTitle | Alterations of cardiac beta-adrenoceptor mechanisms due to calcium depletion and repletion. | lld:pubmed |
| pubmed-article:12030381 | pubmed:affiliation | Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada. | lld:pubmed |
| pubmed-article:12030381 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12030381 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:12030381 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
