ArticleThe Journal of physiology2002
beta-Adrenergic stimulation modulates Ca2+- and voltage-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 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- T-Type Voltage-Gated Calcium Channels: Potential Regulators of Smooth Muscle Contractility.International journal of molecular sciences · 2024Review
- L-type channel inactivation balances the increased peak calcium current due to absence of Rad in cardiomyocytes.The Journal of general physiology · 2021Article
- Impact of phosphomimetic and non-phosphorylatable mutations of phospholemman on L-type calcium channels gating in HEK 293T cells.Journal of cellular and molecular medicine · 2015Article
- Early right ventricular fibrosis and reduction in biventricular cardiac reserve in the dystrophin-deficient mdx heart.American journal of physiology. Heart and circulatory physiology · 2015Article
- Theoretical study of L-type Ca(2+) current inactivation kinetics during action potential repolarization and early afterdepolarizations.The Journal of physiology · 2012Article
- CaBP1 regulates voltage-dependent inactivation and activation of Ca(V)1.2 (L-type) calcium channels.The Journal of biological chemistry · 2011Article
- Phospholemman modulates the gating of cardiac L-type calcium channels.Biophysical journal · 2010Article
- Complex modulation of L-type Ca(2+) current inactivation by sorcin in isolated rabbit cardiomyocytes.Pflugers Archiv : European journal of physiology · 2009Article
- Calsequestrin mutation and catecholaminergic polymorphic ventricular tachycardia: a simulation study of cellular mechanism.Cardiovascular research · 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
- A 3D Monte Carlo analysis of the role of dyadic space geometry in spark generation.Biophysical journal · 2006Article
- Physiological modulation of inactivation in L-type Ca2+ channels: one switch.The Journal of physiology · 2004Review
- Functional roles of cytoplasmic loops and pore lining transmembrane helices in the voltage-dependent inactivation of HVA calcium channels.The Journal of physiology · 2004Review
- L-type Ca2+ channels serve as a sensor of the SR Ca2+ for tuning the efficacy of Ca2+-induced Ca2+ release in rat ventricular myocytes.The Journal of physiology · 2003Article
- Ca2+ entry-dependent inactivation of L-type Ca current: a novel formulation for cardiac action potential models.Biophysical journal · 2003Article
- Beta-adrenergic and muscarinic agonists modulate inactivation of L-type Ca2+ channel currents in guinea-pig ventricular myocytes.The Journal of physiology · 2002Article
- Voltage-dependent inactivation of L-type Ca2+ currents in guinea-pig ventricular myocytes.The Journal of physiology · 2002Article
- Modulation of inactivation of cardiac L-type Ca2+ channels.The Journal of physiology · 2002Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The objective of this study was to examine the effect of beta-adrenergic stimulation upon voltage- and Ca2+-induced inactivation of native cardiac L-type Ca2+ channels. Whole-cell currents were recorded from guinea-pig isolated ventricular myocytes. Total and voltage-dependent inactivation was separated by replacing extracellular Ca2+ with Mg2+. L-type Ca2+ channel behaviour was monitored with outward Ca2+ channel currents. First, the voltage dependence of inactivation was studied at fixed times (50 and 1000 ms) after activation. This showed that under control conditions Ca2+ contributed little to inactivation. In isoproterenol (isoprenaline), voltage-dependent inactivation was markedly reduced and Ca2+ contributed largely to total inactivation. Second, the time dependence of inactivation was studied at a fixed voltage (+10 mV). In control conditions the fast phase of inactivation (tau(f) approximately 15 ms) was reduced to the same extent by ryanodine (tau(f) approximately 30 ms) and the absence of Ca2+ (tau(f) approximately 30 ms) while the slow phase of inactivation (tau(s) approximately 70 ms) was reduced by ryanodine (tau(s) approximately 160 ms) and further reduced in the absence of Ca2+ (tau(s) approximately 300 ms). In isoproterenol, biphasic inactivation of Ca2+ currents (tau(f) approximately 4 ms, tau(s) approximately 60 ms) was replaced by a single slow (tau approximately 450 ms) phase of inactivation in the absence of Ca2+. It is concluded that, under control conditions Ca2+ channel current decay is largely dominated by rapid voltage-dependent inactivation, while in isoproterenol this is replaced by Ca2+-induced inactivation.
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