ArticleJournal of molecular and cellular cardiology2012
Physiological consequences of transient outward K+ current activation during heart failure in the canine left ventricle.
Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 36 citations in OpenAlex.
- The Kv4 potassium channel modulator NS5806 attenuates cardiac hypertrophy in vivo and in vitro.Scientific reports · 2024Article
- Improved CaJournal of molecular and cellular cardiology · 2022Article
- Article
- Arrhythmogenic Remodeling in the Failing Heart.Cells · 2021Review
- Canine Myocytes Represent a Good Model for Human Ventricular Cells Regarding Their Electrophysiological Properties.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Data-Driven Uncertainty Quantification for Cardiac Electrophysiological Models: Impact of Physiological Variability on Action Potential and Spiral Wave Dynamics.Frontiers in physiology · 2020Article
- Comprehensive Uncertainty Quantification and Sensitivity Analysis for Cardiac Action Potential Models.Frontiers in physiology · 2019Article
- Interventricular differences in sodium current and its potential role in Brugada syndrome.Physiological reports · 2018Article
- Regulation of Kv4.3 and hERG potassium channels by KChIP2 isoforms and DPP6 and response to the dual KBiochemical pharmacology · 2018Article
- Differential responses of rabbit ventricular and atrial transient outward current (IPhysiological reports · 2017Article
- Electronegative LDL-mediated cardiac electrical remodeling in a rat model of chronic kidney disease.Scientific reports · 2017Article
- Myocardial KChIP2 Expression in Guinea Pig Resolves an Expanded Electrophysiologic Role.PloS one · 2016Article
- Repolarization Alternans and Ventricular Arrhythmia in a Repaired Tetralogy of Fallot Animal Model.Journal of the American Heart Association · 2015Article
- Regional variation of the inwardly rectifying potassium current in the canine heart and the contributions to differences in action potential repolarization.Journal of molecular and cellular cardiology · 2015Article
- Repolarization reserve evolves dynamically during the cardiac action potential: effects of transient outward currents on early afterdepolarizations.Circulation. Arrhythmia and electrophysiology · 2015Article
- Novel mechanism of transient outward potassium channel current regulation in the heart: implications for cardiac electrophysiology in health and disease.Circulation research · 2015Article
- Modulation of the voltage-gated potassium channel (Kv4.3) and the auxiliary protein (KChIP3) interactions by the current activator NS5806.The Journal of biological chemistry · 2014Article
- Ranolazine effectively suppresses atrial fibrillation in the setting of heart failure.Circulation. Heart failure · 2014Article
- Development of heart failure is independent of K+ channel-interacting protein 2 expression.The Journal of physiology · 2013Article
- Tissue-specific effects of acetylcholine in the canine heart.American journal of physiology. Heart and circulatory physiology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundRemodeling of ion channel expression is well established in heart failure (HF). We determined the extent to which I(to) is reduced in tachypacing-induced HF and assessed the ability of an I(to) activator (NS5806) to recover this current. METHOD AND
resultsWhole-cell patch clamp was used to record I(to) in epicardial (Epi) ventricular myocytes. Epi- and endocardial action potentials were recorded from left ventricular wedge preparations. Right ventricular tachypacing-induced heart failure reduced I(to) density in Epi myocytes (Control=22.1±1.9pA/pF vs 16.1±1.4 after 2weeks and 10.7±1.4pA/pF after 5 weeks, +50mV). Current decay as well as recovery of I(to) from inactivation progressively slowed with the development of heart failure. Reduction of I(to) density was paralleled by a reduction in phase 1 magnitude, epicardial action potential notch and J wave amplitude recorded from coronary-perfused left ventricular wedge preparations. NS5806 increased I(to) (at +50mV) from 16.1±1.4 to 23.9±2.1pA/pF (p<0.05) at 2weeks and from 10.7±1.4 to 14.4±1.9pA/pF (p<0.05) in 5 weeks tachypaced dogs. NS5806 increased both fast and slow phases of I(to) recovery in 2 and 5-week HF cells and restored the action potential notch and J wave in wedge preparations from HF dogs.
conclusionsThe I(to) agonist NS5806 increases the rate of recovery and density of I(to), thus reversing the HF-induced reduction in these parameters. In wedge preparations from HF dogs, NS5806 restored the spike-and-dome morphology of the Epi action potential providing proof of principal that some aspects of electrical remodelling during HF can be pharmacologically reversed.
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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.