ArticleJournal of molecular and cellular cardiology2013
Dynamics of the late Na(+) current during cardiac action potential and its contribution to afterdepolarizations.
Article in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 97 citations in OpenAlex.
- Targeting Arrhythmogenic Late Sodium Current by FHF1Circulation research · 2026Article
- Amiodarone irrecoverably impairs the function of human ether-a-go-go-related gene potassium channels.Molecular pharmacology · 2026Article
- MOG1medRxiv : the preprint server for health sciences · 2025Article
- Article
- Role of dynamical instability in QT interval variability and early afterdepolarization propensity.Biophysical journal · 2025Article
- A novel computational model of swine ventricular myocyte reveals new insights into disease mechanisms and therapeutic approaches in Timothy Syndrome.Scientific reports · 2024Article
- Empagliflozin rescues pro-arrhythmic and CaScientific reports · 2024Article
- Selective Inhibition of Cardiac Late NaBiomedicines · 2023Article
- Conductance Changes of NaPharmaceuticals (Basel, Switzerland) · 2023Article
- Antiarrhythmic and Inotropic Effects of Selective NaInternational journal of molecular sciences · 2022Review
- Modeling cardiomyocyte mechanics and autoregulation of contractility by mechano-chemo-transduction feedback.iScience · 2022Article
- Fibroblast growth factor homologous factors serve as a molecular rheostat in tuning arrhythmogenic cardiac late sodium current.Nature cardiovascular research · 2022Article
- Late Sodium Current of the Heart: Where Do We Stand and Where Are We Going?Pharmaceuticals (Basel, Switzerland) · 2022Review
- Engineered bacterial voltage-gated sodium channel platform for cardiac gene therapy.Nature communications · 2022Article
- Exploring the Coordination of Cardiac Ion Channels With Action Potential Clamp Technique.Frontiers in physiology · 2022Review
- Late sodium current and calcium homeostasis in arrhythmogenesis.Channels (Austin, Tex.) · 2021Review
- Late NaPharmaceuticals (Basel, Switzerland) · 2021Article
- Cardiomyocyte NaBasic research in cardiology · 2021Article
- Calcium Signaling Silencing in Atrial Fibrillation: Implications for Atrial Sodium Homeostasis.International journal of molecular sciences · 2021Review
- Canine Myocytes Represent a Good Model for Human Ventricular Cells Regarding Their Electrophysiological Properties.Pharmaceuticals (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The objective of this work is to examine the contribution of late Na(+) current (INa,L) to the cardiac action potential (AP) and arrhythmogenic activities. In spite of the rapidly growing interest toward this current, there is no publication available on experimental recording of the dynamic INa,L current as it flows during AP with Ca(2+) cycling. Also unknown is how the current profile changes when the Ca(2+)-calmodulin dependent protein kinase II (CaMKII) signaling is altered, and how the current contributes to the development of arrhythmias. In this study we use an innovative AP-clamp Sequential Dissection technique to directly record the INa,L current during the AP with Ca(2+) cycling in the guinea pig ventricular myocytes. First, we found that the magnitude of INa,L measured under AP-clamp is substantially larger than earlier studies indicated. CaMKII inhibition using KN-93 significantly reduced the current. Second, we recorded INa,L together with IKs, IKr, and IK1 in the same cell to understand how these currents counterbalance to shape the AP morphology. We found that the amplitude and the total charge carried by INa,L exceed that of IKs. Third, facilitation of INa,L by Anemone toxin II prolonged APD and induced Ca(2+) oscillations that led to early and delayed afterdepolarizations and triggered APs; these arrhythmogenic activities were eliminated by buffering Ca(2+) with BAPTA. In conclusion, INa,L contributes a significantly large inward current that prolongs APD and unbalances the Ca(2+) homeostasis to cause arrhythmogenic APs.
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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.