Altered Na+ channels promote pause-induced spontaneous diastolic activity in long QT syndrome type 3 myocytes.
about
Impaired endocytosis of the ion channel TRPM4 is associated with human progressive familial heart block type INa⁺ transport in the normal and failing heart - remember the balanceThe late Na+ current--origin and pathophysiological relevanceNew treatment options for late Na current, arrhythmias, and diastolic dysfunctionRole of sodium and calcium dysregulation in tachyarrhythmias in sudden cardiac death.Modeling tissue- and mutation- specific electrophysiological effects in the long QT syndrome: role of the Purkinje fiberMutation-specific risk in two genetic forms of type 3 long QT syndrome.Cardiac Ion Channel Regulation in Obesity and the Metabolic Syndrome: Relevance to Long QT Syndrome and Atrial FibrillationAutonomic modulation and antiarrhythmic therapy in a model of long QT syndrome type 3Electrophysiological characteristics of canine superior vena cava sleeve preparations: effect of ranolazine.Purkinje Cells as Sources of Arrhythmias in Long QT Syndrome Type 3.The cardiac persistent sodium current: an appealing therapeutic target?Na+ transport in cardiac myocytes; Implications for excitation-contraction coupling.Diastolic transient inward current in long QT syndrome type 3 is caused by Ca2+ overload and inhibited by ranolazinePathophysiology of the cardiac late Na current and its potential as a drug target.The arrhythmogenic consequences of increasing late INa in the cardiomyocyte.Abnormalities of calcium metabolism and myocardial contractility depression in the failing heart.Ranolazine for congenital and acquired late INa-linked arrhythmias: in silico pharmacological screening.Timely recognition of cardiovascular toxicity by anticancer agents: a common objective of the pharmacologist, oncologist and cardiologist.Mouse Models of SCN5A-Related Cardiac ArrhythmiasSelective inhibition of persistent sodium current by F 15845 prevents ischaemia-induced arrhythmias.Intracellular calcium attenuates late current conducted by mutant human cardiac sodium channels.An increase of late sodium current induces delayed afterdepolarizations and sustained triggered activity in atrial myocytes.A computational model of Purkinje fibre single cell electrophysiology: implications for the long QT syndrome.Variants: Association With Cardiac Disorders
P2860
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P2860
Altered Na+ channels promote pause-induced spontaneous diastolic activity in long QT syndrome type 3 myocytes.
description
2006 nî lūn-bûn
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2006年の論文
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2006年論文
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2006年論文
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2006年論文
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2006年論文
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name
Altered Na+ channels promote p ...... g QT syndrome type 3 myocytes.
@ast
Altered Na+ channels promote p ...... g QT syndrome type 3 myocytes.
@en
type
label
Altered Na+ channels promote p ...... g QT syndrome type 3 myocytes.
@ast
Altered Na+ channels promote p ...... g QT syndrome type 3 myocytes.
@en
prefLabel
Altered Na+ channels promote p ...... g QT syndrome type 3 myocytes.
@ast
Altered Na+ channels promote p ...... g QT syndrome type 3 myocytes.
@en
P2093
P2860
P1433
P1476
Altered Na+ channels promote p ...... g QT syndrome type 3 myocytes.
@en
P2093
Kevin J Sampson
Nicolas Lindegger
Robert S Kass
Sandra Fredj
P2860
P304
P356
10.1161/01.RES.0000251305.25604.B0
P577
2006-11-02T00:00:00Z