A transient outward potassium current activator recapitulates the electrocardiographic manifestations of Brugada syndrome.
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Multiple arrhythmic syndromes in a newborn, owing to a novel mutation in SCN5ANeuronal and Cardiovascular Potassium Channels as Therapeutic Drug Targets: Promise and PitfallsAcute alterations of somatodendritic action potential dynamics in hippocampal CA1 pyramidal cells after kainate-induced status epilepticus in miceTransient outward current (I(to)) gain-of-function mutations in the KCND3-encoded Kv4.3 potassium channel and Brugada syndromeEffect of Wenxin Keli and quinidine to suppress arrhythmogenesis in an experimental model of Brugada syndrome.Mode of onset of ventricular fibrillation in patients with early repolarization pattern vs. Brugada syndromeDifferential effects of the transient outward K(+) current activator NS5806 in the canine left ventricleAbnormal repolarization as the basis for late potentials and fractionated electrograms recorded from epicardium in experimental models of Brugada syndrome.KCNE2 modulation of Kv4.3 current and its potential role in fatal rhythm disorders.Effect of the I(to) activator NS5806 on cloned K(V)4 channels depends on the accessory protein KChIP2.Quinidine depresses the transmural electrical heterogeneity of transient outward potassium current of the right ventricular outflow tract free wall.Modulation of the voltage-gated potassium channel (Kv4.3) and the auxiliary protein (KChIP3) interactions by the current activator NS5806.Reduced sialylation impacts ventricular repolarization by modulating specific K+ channel isoforms distinctly.Comparison of the effects of a transient outward potassium channel activator on currents recorded from atrial and ventricular cardiomyocytesKv4.3-Encoded Fast Transient Outward Current Is Presented in Kv4.2 Knockout Mouse Cardiomyocytes.Repolarization reserve evolves dynamically during the cardiac action potential: effects of transient outward currents on early afterdepolarizations.Impact of KChIP2 on Cardiac Electrophysiology and the Progression of Heart Failure.Physiological consequences of transient outward K+ current activation during heart failure in the canine left ventricle.Ionic and cellular mechanisms underlying the development of acquired Brugada syndrome in patients treated with antidepressants.Reductions in the Cardiac Transient Outward K+ Current Ito Caused by Chronic β-Adrenergic Receptor Stimulation Are Partly Rescued by Inhibition of Nuclear Factor κB.Characterization of SEMA3A-encoded semaphorin as a naturally occurring Kv4.3 protein inhibitor and its contribution to Brugada syndrome.The genetic component of Brugada syndromeCellular mechanisms underlying the effects of milrinone and cilostazol to suppress arrhythmogenesis associated with Brugada syndrome.Dependence of phase-2 reentry and repolarization dispersion on epicardial and transmural ionic heterogeneity: a simulation study.Genetic, molecular and cellular mechanisms underlying the J wave syndromes.Optical and electrical recordings from isolated coronary-perfused ventricular wedge preparations.Cardiac potassium channel subtypes: new roles in repolarization and arrhythmia.Kvβ1.1 (AKR6A8) senses pyridine nucleotide changes in the mouse heart and modulates cardiac electrical activity.Novel mechanism of transient outward potassium channel current regulation in the heart: implications for cardiac electrophysiology in health and disease.The pathophysiological mechanism underlying Brugada syndrome: depolarization versus repolarizationDifferential responses of rabbit ventricular and atrial transient outward current (Ito) to the Ito modulator NS5806.The acquired Brugada syndrome and the paradox of choice.Regional variations in action potential alternans in isolated murine Scn5a (+/-) hearts during dynamic pacing.Loss of K+ currents in heart failure is accentuated in KChIP2 deficient mice.A novel KCND3 gain-of-function mutation associated with early-onset of persistent lone atrial fibrillation.Regulation of Kv4.3 and hERG potassium channels by KChIP2 isoforms and DPP6 and response to the dual K+ channel activator NS3623.NS5806 partially restores action potential duration but fails to ameliorate calcium transient dysfunction in a computational model of canine heart failure.Regulation and physiological function of Nav1.5 and KCNQ1 channels
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A transient outward potassium current activator recapitulates the electrocardiographic manifestations of Brugada syndrome.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 10 December 2008
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
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name
A transient outward potassium ...... estations of Brugada syndrome.
@en
A transient outward potassium ...... estations of Brugada syndrome.
@nl
type
label
A transient outward potassium ...... estations of Brugada syndrome.
@en
A transient outward potassium ...... estations of Brugada syndrome.
@nl
prefLabel
A transient outward potassium ...... estations of Brugada syndrome.
@en
A transient outward potassium ...... estations of Brugada syndrome.
@nl
P2093
P2860
P50
P356
P1476
A transient outward potassium ...... festations of Brugada syndrome
@en
P2093
Jonathan M Cordeiro
José M Di Diego
Morten Grunnet
Rie S Hansen
P2860
P304
P356
10.1093/CVR/CVN339
P577
2008-12-10T00:00:00Z