ArticlePflugers Archiv : European journal of physiology2013
[Ca²⁺] i-induced augmentation of the inward rectifier potassium current (IK1) in canine and human ventricular myocardium.
Article in Pflugers Archiv : European journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Beta-Adrenergic Activation of the Inward Rectifier KInternational journal of molecular sciences · 2024Article
- The network of cardiac KNaunyn-Schmiedeberg's archives of pharmacology · 2024Review
- In silico analysis of the contribution of cardiomyocyte-fibroblast electromechanical interaction to the arrhythmia.Frontiers in physiology · 2023Article
- A NovelFrontiers in physiology · 2022Article
- Arrhythmogenic Remodeling in the Failing Heart.Cells · 2021Review
- ESC working group on cardiac cellular electrophysiology position paper: relevance, opportunities, and limitations of experimental models for cardiac electrophysiology research.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2021Review
- Immediate and Delayed Response of Simulated Human Atrial Myocytes to Clinically-Relevant Hypokalemia.Frontiers in physiology · 2021Article
- Simulation of the Effects of Extracellular Calcium Changes Leads to a Novel Computational Model of Human Ventricular Action Potential With a Revised Calcium Handling.Frontiers in physiology · 2020Article
- Conduction in the right and left ventricle is differentially regulated by protein kinases and phosphatases: implications for arrhythmogenesis.American journal of physiology. Heart and circulatory physiology · 2019Article
- Calcium/calmodulin-dependent protein kinase II regulation of IHeart rhythm · 2018Article
- Altered Repolarization Reserve in Failing Rabbit Ventricular Myocytes: Calcium and β-Adrenergic Effects on Delayed- and Inward-Rectifier Potassium Currents.Circulation. Arrhythmia and electrophysiology · 2018Article
- Estimating the probabilities of rare arrhythmic events in multiscale computational models of cardiac cells and tissue.PLoS computational biology · 2017Article
- The inward rectifier current inhibitor PA-6 terminates atrial fibrillation and does not cause ventricular arrhythmias in goat and dog models.British journal of pharmacology · 2017Article
- Electrophysiologic effects of the IK1 inhibitor PA-6 are modulated by extracellular potassium in isolated guinea pig hearts.Physiological reports · 2017Article
- Effects of zacopride, a moderate IPharmacological research · 2017Article
- Ion channelopathies in human induced pluripotent stem cell derived cardiomyocytes: a dynamic clamp study with virtual IK1.Frontiers in physiology · 2015Article
- Selective Na(+) /Ca(2+) exchanger inhibition prevents Ca(2+) overload-induced triggered arrhythmias.British journal of pharmacology · 2014Article
- Human atrial cell models to analyse haemodialysis-related effects on cardiac electrophysiology: work in progress.Computational and mathematical methods in medicine · 2014Review
- CaMKII regulation of cardiac K channels.Frontiers in pharmacology · 2014Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inward rectifier K⁺ current (IK1) plays an important role in terminal repolarization and stabilization of the resting potential in cardiac cells. Although IK1 was shown to be sensitive to changes in intracellular Ca²⁺ concentration ([Ca²⁺]i), the nature of this Ca²⁺ sensitivity-in spite of its deep influence on action potential morphology-is controversial. Therefore, we aimed to investigate the effects of a nonadrenergic rise in [Ca²⁺]i on the amplitude of IK1 in canine and human ventricular myocardium and its consequences on cardiac repolarization. IK1, defined as the current inhibited by 10 μM Ba²⁺, was significantly increased in isolated canine myocytes following a steady rise in [Ca²⁺]i. Enhanced IK1 was also observed when [Ca²⁺]i was not buffered by ethylene glycol tetraacetic acid, and [Ca²⁺]I transients were generated. This [Ca²⁺]i-dependent augmentation of IK1 was largely attenuated after inhibition of CaMKII by 1 μM KN-93. Elevation of [Ca²⁺]o in multicellular canine and human ventricular preparations resulted in shortening of action potentials and acceleration of terminal repolarization. High [Ca²⁺]o enhanced the action potential lengthening effect of the Ba(2+)-induced IK1 blockade and attenuated the prolongation of action potentials following a 0.3-μM dofetilide-induced IKr blockade. Blockade of IKs by 0.5 μM HMR-1556 had no significant effect on APD90 in either 2 mM or 4 mM [Ca²⁺]o. It is concluded that high [Ca²⁺]i leads to augmentation of the Ba²⁺-sensitive current in dogs and humans, regardless of the mechanism of the increase. This effect seems to be at least partially mediated by a CaMKII-dependent pathway and may provide an effective endogenous defense against cardiac arrhythmias induced by Ca²⁺ overload.
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