Linked Life Data

11208562

Source:http://linkedlifedata.com/resource/pubmed/id/11208562

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-3-14
pubmed:abstractText
To corroborate alterations in the functional responses to beta-adrenergic receptor (beta-AR) stimulation with changes in beta-AR signaling in failing cardiomyocytes, contractile and L-type Ca(2+) current responses to isoproterenol along with stimulated cAMP generation were compared among cardiomyocytes isolated from canines with tachycardia-induced heart failure or healthy hearts. The magnitude of shortening of failing cardiomyocytes was significantly depressed (by 22 +/- 4.4%) under basal conditions, and the maximal response to isoproterenol was significantly reduced (by 45 +/- 18%). Similar results were obtained when the responses in the rate of contraction and rate of relaxation to isoproterenol were considered. The L-type Ca(2+) current amplitude measured in failing cardiomyocytes under basal conditions was unchanged, but the responses to isoproterenol were significantly reduced compared with healthy cells. Isoproterenol-stimulated cAMP generation was similar in sarcolemmal membranes derived from the homogenates of failing (45 +/- 6.8) and healthy cardiomyocytes (52 +/- 8.5 pmol cAMP. mg protein(-1). min(-1)). However, stimulated cAMP generation was found to be significantly reduced when the membranes were derived from the homogenates of whole tissue (failing: 67 +/- 8.1 vs. healthy: 140 +/- 27.8 pmol cAMP. mg protein(-1). min(-1)). Total beta-AR density was not reduced in membranes derived from either whole tissue or isolated cardiomyocyte homogenates, but the beta(1)/beta(2) ratio was significantly reduced in the former (failing: 45/55 vs. healthy: 72/28) without being altered in the latter (failing: 72/28, healthy: 77/23). We thus conclude that, in tachycardia-induced heart failure, reduction in the functional responses of isolated cardiomyocytes to beta-AR stimulation may be attributed to alterations in the excitation-contraction machinery rather than to limitation of cAMP generation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0363-6119
pubmed:author
pubmed:issnType
Print
pubmed:volume
280
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R355-64
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:11208562-1-Methyl-3-isobutylxanthine, pubmed-meshheading:11208562-Adenylate Cyclase, pubmed-meshheading:11208562-Animals, pubmed-meshheading:11208562-Calcium Channels, L-Type, pubmed-meshheading:11208562-Cell Membrane, pubmed-meshheading:11208562-Cells, Cultured, pubmed-meshheading:11208562-Cyclic AMP, pubmed-meshheading:11208562-Dogs, pubmed-meshheading:11208562-Female, pubmed-meshheading:11208562-Heart, pubmed-meshheading:11208562-Heart Failure, pubmed-meshheading:11208562-Isoproterenol, pubmed-meshheading:11208562-Male, pubmed-meshheading:11208562-Membrane Potentials, pubmed-meshheading:11208562-Myocardial Contraction, pubmed-meshheading:11208562-Myocardium, pubmed-meshheading:11208562-Norepinephrine, pubmed-meshheading:11208562-Receptors, Adrenergic, beta, pubmed-meshheading:11208562-Reference Values, pubmed-meshheading:11208562-Signal Transduction, pubmed-meshheading:11208562-Tachycardia
pubmed:year
2001
pubmed:articleTitle
Functional desensitization to isoproterenol without reducing cAMP production in canine failing cardiocytes.
pubmed:affiliation
Département de Pharmacologie, Faculté de Médecine, Université de Montréal, Québec H3C 3J7, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't