ArticleThe Journal of physiology2012
Transient outward K+ current reduction prolongs action potentials and promotes afterdepolarisations: a dynamic-clamp study in human and rabbit cardiac atrial myocytes.
Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Macrophage Immunometabolism in Epicardial Adipose Tissue and Obesity-Related Atrial Fibrillation.Journal of inflammation research · 2026Review
- Article
- Quantitative assessment of the usability of electromechanical human-based modelling and simulation to replace Langendorff isolated rabbit heart experiments in the preclinical setting.Frontiers in pharmacology · 2025Article
- Modeling Fibroblast-Cardiomyocyte Interactions: Unveiling the Role of Ion Currents in Action Potential Modulation.International journal of molecular sciences · 2024Article
- Global Air Pollutant Phenanthrene and Arrhythmic Outcomes in a Mouse Model.Environmental health perspectives · 2023Article
- Cardiac Alternans: From Bedside to Bench and Back.Circulation research · 2023Review
- Acute Genetic Ablation of Cardiac Sodium/Calcium Exchange in Adult Mice: Implications for Cardiomyocyte Calcium Regulation, Cardioprotection, and Arrhythmia.Journal of the American Heart Association · 2021Article
- Cardioprotection by SGLT2 Inhibitors-Does It All Come Down to NaInternational journal of molecular sciences · 2021Review
- Patch-Clamp Recordings of Action Potentials From Human Atrial Myocytes: Optimization Through Dynamic Clamp.Frontiers in pharmacology · 2021Article
- Inhibition of cardiac potassium currents by oxidation-activated protein kinase A contributes to early afterdepolarizations in the heart.American journal of physiology. Heart and circulatory physiology · 2020Article
- Arrhythmia mechanisms and spontaneous calcium release: Bi-directional coupling between re-entrant and focal excitation.PLoS computational biology · 2019Article
- Dynamic clamping human and rabbit atrial calcium current: narrowing IThe Journal of physiology · 2019Article
- Transient outward KAmerican journal of physiology. Heart and circulatory physiology · 2019Article
- IJournal of physiology and biochemistry · 2018Article
- Description of the Human Atrial Action Potential Derived From a Single, Congruent Data Source: Novel Computational Models for Integrated Experimental-Numerical Study of Atrial Arrhythmia Mechanisms.Frontiers in physiology · 2018Article
- Applications of Dynamic Clamp to Cardiac Arrhythmia Research: Role in Drug Target Discovery and Safety Pharmacology Testing.Frontiers in physiology · 2017Review
- Mechanisms of cardiac arrhythmias.Journal of arrhythmia · 2016Review
- Genome-wide screening identifies a KCNIP1 copy number variant as a genetic predictor for atrial fibrillation.Nature communications · 2016Article
- Atrial Electrophysiological Remodeling and Fibrillation in Heart Failure.Clinical Medicine Insights. Cardiology · 2016Review
- Neuronal and Cardiovascular Potassium Channels as Therapeutic Drug Targets: Promise and Pitfalls.Journal of biomolecular screening · 2015Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human atrial transient outward K(+) current (I(TO)) is decreased in a variety of cardiac pathologies, but how I(TO) reduction alters action potentials (APs) and arrhythmia mechanisms is poorly understood, owing to non-selectivity of I(TO) blockers. The aim of this study was to investigate effects of selective I(TO) changes on AP shape and duration (APD), and on afterdepolarisations or abnormal automaticity with β-adrenergic-stimulation, using the dynamic-clamp technique in atrial cells. Human and rabbit atrial cells were isolated by enzymatic dissociation, and electrical activity recorded by whole-cell-patch clamp (35-37°C). Dynamic-clamp-simulated I(TO) reduction or block slowed AP phase 1 and elevated the plateau, significantly prolonging APD, in both species. In human atrial cells, I(TO) block (100% I(TO) subtraction) increased APD(50) by 31%, APD(90) by 17%, and APD(-61 mV) (reflecting cellular effective refractory period) by 22% (P < 0.05 for each). Interrupting I(TO) block at various time points during repolarisation revealed that the APD(90) increase resulted mainly from plateau-elevation, rather than from phase 1-slowing or any residual I(TO). In rabbit atrial cells, partial I(TO) block (∼40% I(TO) subtraction) reversibly increased the incidence of cellular arrhythmic depolarisations (CADs; afterdepolarisations and/or abnormal automaticity) in the presence of the β-agonist isoproterenol (0.1 μm; ISO), from 0% to 64% (P < 0.05). ISO-induced CADs were significantly suppressed by dynamic-clamp increase in I(TO) (∼40% I(TO) addition). ISO+I(TO) decrease-induced CADs were abolished by β(1)-antagonism with atenolol at therapeutic concentration (1 μm). Atrial cell action potential changes from selective I(TO) modulation, shown for the first time using dynamic-clamp, have the potential to influence reentrant and non-reentrant arrhythmia mechanisms, with implications for both the development and treatment of atrial fibrillation.
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