ReviewThe Journal of physiology2004
Physiological modulation of inactivation in L-type Ca2+ channels: one switch.
Review in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 69 citations in OpenAlex.
- Phosphoinositide Depletion and Compensatory Phospho-Signaling in Angiotensin II-Induced Heart Disease.Circulation research · 2026Article
- Aberrant myocardial calcium cycling: pathogenic mechanisms and targeted therapeutics for heart failure.Frontiers in cardiovascular medicine · 2026Review
- Models of the cardiac L-type calcium current: A quantitative review.WIREs mechanisms of disease · 2023Review
- Targeting late ICaL to close the window to ventricular arrhythmias.The Journal of general physiology · 2021Article
- L-type channel inactivation balances the increased peak calcium current due to absence of Rad in cardiomyocytes.The Journal of general physiology · 2021Article
- Calcium-dependent inactivation controls cardiac L-type CaThe Journal of general physiology · 2019Article
- How CaThe Journal of general physiology · 2019Article
- Mutations in voltage-gated L-type calcium channel: implications in cardiac arrhythmia.Channels (Austin, Tex.) · 2018Review
- Identification of Na+/K+-ATPase inhibition-independent proarrhythmic ionic mechanisms of cardiac glycosides.Scientific reports · 2017Article
- L-Type Calcium Channel Inhibition Contributes to the Proarrhythmic Effects of Aconitine in Human Cardiomyocytes.PloS one · 2017Article
- Rational strategy to stop arrhythmias: Early afterdepolarizations and L-type Ca2+ current.The Journal of general physiology · 2015Article
- Expression profile analysis of circulating microRNAs and their effects on ion channels in Chinese atrial fibrillation patients.International journal of clinical and experimental medicine · 2015Article
- Computer simulation of voltage sensitive calcium ion channels in a dendritic spine.Journal of theoretical biology · 2013Article
- Defective calcium inactivation causes long QT in obese insulin-resistant rat.American journal of physiology. Heart and circulatory physiology · 2012Article
- Calcineurin Controls Voltage-Dependent-Inactivation (VDI) of the Normal and Timothy Cardiac Channels.Scientific reports · 2012Article
- Influence of pH on Ca²⁺ current and its control of electrical and Ca²⁺ signaling in ventricular myocytes.The Journal of general physiology · 2011Article
- Negative feedback regulation of microbe-associated molecular pattern-induced cytosolic Ca2+ transients by protein phosphorylation.Journal of plant research · 2011Article
- L-type calcium channel auto-regulation of transcription.Cell calcium · 2011Review
- CaBP1 regulates voltage-dependent inactivation and activation of Ca(V)1.2 (L-type) calcium channels.The Journal of biological chemistry · 2011Article
- Synaptic vesicles control the time course of neurotransmitter secretion via a Ca²+/H+ antiport.The Journal of physiology · 2011Article
Corrections and comments
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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 relative contributions of voltage- and Ca(2+)-dependent mechanisms of inactivation to the decay of L-type Ca(2+) channel currents (I(CaL)) is an old story to which recent results have given an unexpected twist. In cardiac myocytes voltage-dependent inactivation (VDI) was thought to be slow and Ca(2+)-dependent inactivation (CDI) resulting from Ca(2+) influx and Ca(2+)-induced Ca(2+)-release (CICR) from the sarcoplasmic reticulum provided an automatic negative feedback mechanism to limit Ca(2+) entry and the contribution of I(CaL) to the cardiac action potential. Physiological modulation of I(CaL) by Beta-adrenergic and muscarinic agonists then involved essentially more or less of the same by enhancing or reducing Ca(2+) channel activity, Ca(2+) influx, sarcoplasmic reticulum load and thus CDI. Recent results on the other hand place VDI at the centre of the regulation of I(CaL). Under basal conditions it has been found that depolarization increases the probability that an ion channel will show rapid VDI. This is prevented by Beta-adrenergic stimulation. Evidence also suggests that a channel which shows rapid VDI inactivates before CDI can become effective. Therefore the contributions of VDI and CDI to the decay of I(CaL) are determined by the turning on, by depolarization, and the turning off, by phosphorylation, of the mechanism of rapid VDI. The physiological implications of these ideas are that under basal conditions the contribution of I(CaL) to the action potential will be determined largely by voltage and by Ca(2+) following Beta-adrenergic stimulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.