ReviewBritish journal of pharmacology2008
The cardiac persistent sodium current: an appealing therapeutic target?
Review in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 116 citations in OpenAlex.
- Efficacy of sodium channel blockers in treating myotonia is independent of action potential sodium current block.The Journal of physiology · 2026Article
- A Possible Role of Tetrodotoxin-Sensitive NaInternational journal of molecular sciences · 2024Article
- Ranolazine for improving coronary microvascular function in patients with nonobstructive coronary artery disease: a systematic review and meta-analysis with a trial sequential analysis of randomized controlled trials.Quantitative imaging in medicine and surgery · 2024Article
- Increased GIRK channel activity prevents arrhythmia in mice with heart failure by enhancing ventricular repolarization.Scientific reports · 2023Article
- Improvement of Vascular Insulin Sensitivity by Ranolazine.International journal of molecular sciences · 2023Article
- Article
- Cardiac Late Sodium Channel Current Is a Molecular Target for the Sodium/Glucose Cotransporter 2 Inhibitor Empagliflozin.Circulation · 2021Article
- Inhibitory Effect of Eslicarbazepine Acetate and S-Licarbazepine on NaFrontiers in pharmacology · 2020Article
- Ranolazine as an Alternative Therapy to Flecainide for SCN5A V411M Long QT Syndrome Type 3 Patients.Frontiers in pharmacology · 2020Article
- Selective late sodium current inhibitor GS-458967 suppresses Torsades de Pointes by mostly affecting perpetuation but not initiation of the arrhythmia.British journal of pharmacology · 2018Article
- Multiple targets for flecainide action: implications for cardiac arrhythmogenesis.British journal of pharmacology · 2018Review
- Risk of QT prolongation and torsade de pointes associated with exposure to hydroxyzine: re-evaluation of an established drug.Pharmacology research & perspectives · 2017Article
- Sodium channel biophysics, late sodium current and genetic arrhythmic syndromes.Pflugers Archiv : European journal of physiology · 2017Review
- Tolterodine reduces veratridine-augmented late IActa pharmacologica Sinica · 2016Article
- Antagonism of Nav channels and α1-adrenergic receptors contributes to vascular smooth muscle effects of ranolazine.Scientific reports · 2015Article
- Human Na(v)1.8: enhanced persistent and ramp currents contribute to distinct firing properties of human DRG neurons.Journal of neurophysiology · 2015Article
- Synergetic action of domain II and IV underlies persistent current generation in Nav1.3 as revealed by a tarantula toxin.Scientific reports · 2015Article
- Diverse mechanisms underlying the regulation of ion channels by carbon monoxide.British journal of pharmacology · 2015Review
- Late Sodium Current in Human Atrial Cardiomyocytes from Patients in Sinus Rhythm and Atrial Fibrillation.PloS one · 2015Article
- Identifying tinnitus-related genes based on a side-effect network analysis.CPT: pharmacometrics & systems pharmacology · 2014Article
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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 sodium current in the heart is not a single current with a mono-exponential decay but rather a mixture of currents with different kinetics. It is not clear whether these arise from distinct populations of channels, or from modulation of a single population. A very slowly inactivating component, [(INa(P))] I(Na(P)) is usually about 1% of the size of the peak transient current [I(Na(T))], but is enhanced by hypoxia. It contributes to Na(+) loading and cellular damage in ischaemia and re-perfusion, and perhaps to ischaemic arrhythmias. Class I antiarrhythmic agents such as flecainide, lidocaine and mexiletine generally block I(NA(P)) more potently than block of I(Na(T)) and have been used clinically to treat LQT3 syndrome, which arises because mutations in SCN5A produce defective inactivation of the cardiac sodium channel. The same approach may be useful in some pathological situations, such as ischaemic arrhythmias or diastolic dysfunction, and newer agents are being developed with this goal. For example, ranolazine blocks I(Na(P)) about 10 times more potently than I(Na(T)) and has shown promise in the treatment of angina. Alternatively, the combination of I(Na(P)) block with K(+) channel block may provide protection from the induction of Torsades de Pointe when these agents are used to treat atrial arrhythmias (eg Vernakalant). In all of these scenarios, an understanding of the role of I(Na(P)) in cardiac pathophysiology, the mechanisms by which it may affect cardiac electrophysiology and the potential side effects of blocking I(Na(P)) in the heart and elsewhere will become increasingly important.
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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.