Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1991-12-9
pubmed:abstractText
The Ca(2+)-current plays a prominent role in triggering excitation-contraction coupling in the mammalian heart. It is also a target of clinically important drugs such as catecholamines or Ca(2+)-channel blockers. Until now studies of Ca(2+)-channels in human ventricular myocardium have been hampered by the fact that adequate voltage control cannot be obtained in multicellular preparations. To characterize the properties of human myocardial Ca(2+)-currents, ventricular myocytes were isolated from explanted hearts of patients with end-stage heart failure undergoing cardiac transplantation. The current-voltage relation and voltage-dependent inactivation of L-type currents were similar to those in non-diseased guinea-pig myocardium. Currents could be stimulated with isoprenaline in a dose-dependent manner. When cells were superfused with a Na(+)-free solution in the presence of Tetrodotoxin, Cs+ and Tetraethylammonium to block interfering Na+ and K(+)-currents, depolarization from a holding potential of -90 mV to -80-(-)50 mV did not elicit any time-dependent inward-current. Changing the holding potential from -90 to -45 mV did not alter the current-voltage relation. We conclude that T-type Ca(2+)-currents do not seem to make a detectable contribution to the transmembrane Ca(2+)-influx and that L-type currents in human ventricular myocytes of patients with severe heart failure have characteristics that are similar to those in other mammalian species.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-2828
pubmed:author
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
929-37
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Characteristics of calcium-current in isolated human ventricular myocytes from patients with terminal heart failure.
pubmed:affiliation
Department of Medicine I, University of Munich, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't