ArticleThe Journal of physiology2002
Voltage- and cation-dependent inactivation of L-type Ca2+ channel currents in guinea-pig ventricular myocytes.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Calmodulin D133H Disrupts CaCells · 2025Article
- Hesperetin Relaxes Depolarizing Contraction in Human Umbilical Vein by Inhibiting L-Type CaChinese journal of integrative medicine · 2025Article
- Models of the cardiac L-type calcium current: A quantitative review.WIREs mechanisms of disease · 2023Review
- Preferential Expression of CaBiomolecules · 2022Article
- Targeting late ICaL to close the window to ventricular arrhythmias.The Journal of general physiology · 2021Article
- Calcium-dependent inactivation controls cardiac L-type CaThe Journal of general physiology · 2019Article
- Enhanced Depolarization Drive in Failing Rabbit Ventricular Myocytes: Calcium-Dependent and β-Adrenergic Effects on Late Sodium, L-Type Calcium, and Sodium-Calcium Exchange Currents.Circulation. Arrhythmia and electrophysiology · 2019Article
- The Role of Reactive Oxygen Species in β-Adrenergic Signaling in Cardiomyocytes from Mice with the Metabolic Syndrome.PloS one · 2016Article
- Theoretical study of L-type Ca(2+) current inactivation kinetics during action potential repolarization and early afterdepolarizations.The Journal of physiology · 2012Article
- The mechanisms underlying ICa heterogeneity across murine left ventricle.Molecular and cellular biochemistry · 2011Article
- Simulation of the undiseased human cardiac ventricular action potential: model formulation and experimental validation.PLoS computational biology · 2011Article
- Interplay of voltage and Ca-dependent inactivation of L-type Ca current.Progress in biophysics and molecular biology · 2010Review
- Contribution of L-type Ca2+ channels to early afterdepolarizations induced by I Kr and I Ks channel suppression in guinea pig ventricular myocytes.The Journal of membrane biology · 2008Article
- A rabbit ventricular action potential model replicating cardiac dynamics at rapid heart rates.Biophysical journal · 2008Article
- Voltage-dependent calcium channels of dog basilar artery.The Journal of physiology · 2007Article
- Kinetic properties of the cardiac L-type Ca2+ channel and its role in myocyte electrophysiology: a theoretical investigation.Biophysical journal · 2007Article
- The role of constitutive PKA-mediated phosphorylation in the regulation of basal I(Ca) in isolated rat cardiac myocytes.British journal of pharmacology · 2006Article
- Physiological modulation of inactivation in L-type Ca2+ channels: one switch.The Journal of physiology · 2004Review
- Modulation of manganese currents by 1, 4-dihydropyridines, isoproterenol and forskolin in rabbit ventricular cells.Pflugers Archiv : European journal of physiology · 2003Article
- Ca2+ entry-dependent inactivation of L-type Ca current: a novel formulation for cardiac action potential models.Biophysical journal · 2003Article
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Abstract
L-type Ca2+ channel currents in native ventricular myocytes inactivate according to voltage- and Ca2+-dependent processes. This study sought to examine the effect of beta-adrenergic stimulation on the contributions of voltage and Ca2+ to Ca2+ current decay. Ventricular myocytes were enzymatically isolated from guinea-pig hearts. Inward whole-cell Cd2+-sensitive L-type Ca2+ channel currents were recorded with the patch clamp technique and comparison was made between inward currents carried by Ca2+ and either Ba2+, Sr2+ or Na+. In control conditions the decay of Ca2+ currents was faster than Ba2+, Sr2+ or Na+ currents at negative voltages while at positive voltages there was no difference. The relationship between voltage and inactivation for Ca2+ currents was bell-shaped, while that for Ba2+, Sr2+, and Na+ currents was sigmoid. Thus depolarisation progressively replaced Ca2+-dependent inactivation in the fast phase of decay of Ca2+ channel currents with rapid voltage-dependent inactivation. In the presence of isoproterenol (isoprenaline) the decay of Ca2+ currents was faster than Ba2+, Sr2+ or Na+ currents at all measured voltages (-40 to +30 mV). The relationship between voltage and inactivation for Ca2+, Ba2+ and Sr2+ currents was bell-shaped, while that for Na+ currents was sigmoid with less inactivation than under control conditions. Therefore the fast phase of decay of Ca2+ channel currents was now almost entirely due to Ca2+. It is concluded that the relative contributions of Ca2+- and voltage-dependent mechanisms of inactivation of L-type Ca2+ channels in native cardiac myocytes are modulated by beta-adrenergic stimulation influencing the amount of rapid voltage-dependent inactivation.
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