Linked Life Data

12030381

Source:http://linkedlifedata.com/resource/pubmed/id/12030381

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2002-5-27
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0300-8177
pubmed:author
pubmed:issnType
Print
pubmed:volume
232
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
63-73
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Alterations of cardiac beta-adrenoceptor mechanisms due to calcium depletion and repletion.
pubmed:affiliation
Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't