ReviewProgress in biophysics and molecular biology2010
Interplay of voltage and Ca-dependent inactivation of L-type Ca current.
Review in Progress in biophysics and molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Voltage-Gated Calcium Channels and the Parity-Dependent Differential Uterine Response to Oxytocin in Rats.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Bacterial toxins and heart function: heat-labileBiophysical reviews · 2023Article
- Antiarrhythmic and Inotropic Effects of Selective NaInternational journal of molecular sciences · 2022Review
- L-type channel inactivation balances the increased peak calcium current due to absence of Rad in cardiomyocytes.The Journal of general physiology · 2021Article
- Intracellular O-linked glycosylation directly regulates cardiomyocyte L-type CaBasic research in cardiology · 2020Article
- Calcium-dependent inactivation controls cardiac L-type CaThe Journal of general physiology · 2019Article
- How 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
- A Mathematical Model of the Human Cardiac NaThe Journal of membrane biology · 2019Article
- Validation and Trustworthiness of Multiscale Models of Cardiac Electrophysiology.Frontiers in physiology · 2018Review
- Cardioprotective effects of 5-hydroxymethylfurfural mediated by inhibition of L-type CaBritish journal of pharmacology · 2017Article
- Sarcolemmal distribution ofAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Interactions between N and C termini of α1C subunit regulate inactivation of CaV1.2 L-type Ca(2+) channel.Channels (Austin, Tex.) · 2016Article
- Arrhythmogenesis in a catecholaminergic polymorphic ventricular tachycardia mutation that depresses ryanodine receptor function.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Arrhythmogenic mechanisms in ryanodine receptor channelopathies.Science China. Life sciences · 2015Review
- Calmodulin mutations associated with long QT syndrome prevent inactivation of cardiac L-type Ca(2+) currents and promote proarrhythmic behavior in ventricular myocytes.Journal of molecular and cellular cardiology · 2014Article
- Ca(2+) current facilitation is CaMKII-dependent and has arrhythmogenic consequences.Frontiers in pharmacology · 2014Review
- Rad GTPase deletion increases L-type calcium channel current leading to increased cardiac contraction.Journal of the American Heart Association · 2013Article
- Theoretical study of L-type Ca(2+) current inactivation kinetics during action potential repolarization and early afterdepolarizations.The Journal of physiology · 2012Article
- Simulation of the undiseased human cardiac ventricular action potential: model formulation and experimental validation.PLoS computational biology · 2011Article
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5 authors.
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Abstract
Inactivation of L-type Ca channels (LTCC) is regulated by both Ca and voltage-dependent processes (CDI and VDI). To differentiate VDI and CDI, several experimental and theoretical studies have considered the inactivation of Ba current through LTCC (I(Ba)) as a measure of VDI. However, there is evidence that Ba can weakly mimic Ca, such that I(Ba) inactivation is still a mixture of CDI and VDI. To avoid this complication, some have used the monovalent cation current through LTCC (I(NS)), which can be measured when divalent cation concentrations are very low. Notably, I(NS) inactivation rate does not depend on current amplitude, and hence may reflect purely VDI. However, based on analysis of existent and new data, and modeling, we find that I(NS) can inactivate more rapidly and completely than I(Ba), especially at physiological temperature. Thus VDI that occurs during I(Ba) (or I(Ca)) must differ intrinsically from VDI during I(NS). To account for this, we have extended a previously published LTCC mathematical model of VDI and CDI into an excitation-contraction coupling model, and assessed whether and how experimental I(Ba) inactivation results (traditionally used in VDI experiments and models) could be recapitulated by modifying CDI to account for Ba-dependent inactivation. Thus, the view of a slow and incomplete I(NS) inactivation should be revised, and I(NS) inactivation is a poor measure of VDI during I(Ca) or I(Ba). This complicates VDI analysis experimentally, but raises intriguing new questions about how the molecular mechanisms of VDI differ for divalent and monovalent currents through LTCCs.
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