title: Characteristics of calcium-current in isolated human ventricular myocytes from patients with terminal heart failure.
abstract: 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.
authors.affiliation: Department of Medicine I, University of Munich, Germany.
authors.forename: D J
authors.initials: DJ
authors.lastname: Beuckelmann
authors.forename: M
authors.initials: M
authors.lastname: Näbauer
authors.forename: E
authors.initials: E
authors.lastname: Erdmann
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D002311:Cardiomyopathy, Dilated / Q000473:pathology / Q000503:physiopathology*; D002469:Cell Separation; D003327:Coronary Disease / Q000473:pathology / Q000503:physiopathology*; D006352:Heart Ventricles; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology; D009206:Myocardium / Q000473:pathology*
chemical_list: D015220:Calcium Channels; D007545:Isoproterenol