Hypoxia increases persistent sodium current in rat ventricular myocytes.
about
Na⁺ transport in the normal and failing heart - remember the balanceThe role of late I Na in development of cardiac arrhythmiasThe late Na+ current--origin and pathophysiological relevanceNew treatment options for late Na current, arrhythmias, and diastolic dysfunctionAberrant sodium influx causes cardiomyopathy and atrial fibrillation in miceRanolazine improves cardiac diastolic dysfunction through modulation of myofilament calcium sensitivityThe persistent sodium current blocker riluzole is antiarrhythmic and anti-ischaemic in a pig model of acute myocardial infarctionRegulation of breathing and autonomic outflows by chemoreceptors.Contributions of ion channel currents to ventricular action potential changes and induction of early afterdepolarizations during acute hypoxia.Inhibition of the late sodium current slows t-tubule disruption during the progression of hypertensive heart disease in the rat.Role of voltage-gated Na+ channels in hypoxia-induced neuronal injuries.Activity of the Na+/H+ exchanger contributes to cardiac damage following ischaemia and reperfusion.Riluzole protects against cardiac ischaemia and reperfusion damage via block of the persistent sodium current.Resveratrol attenuates the Na(+)-dependent intracellular Ca(2+) overload by inhibiting H(2)O(2)-induced increase in late sodium current in ventricular myocytesLate sodium current in the pathophysiology of cardiovascular disease: consequences of sodium-calcium overload.Direct protective effects of poly-unsaturated fatty acids, DHA and EPA, against activation of cardiac late sodium current: a mechanism for ischemia selectivity.Ranolazine attenuates behavioral signs of neuropathic pain.Remote ischemic preconditioning of cardiomyocytes inhibits the mitochondrial permeability transition pore independently of reduced calcium-loading or sarcKATP channel activation.The role of sodium channel current in modulating transmural dispersion of repolarization and arrhythmogenesis.Effects of ranolazine on torsades de pointes tachycardias in a healthy isolated rabbit heart modelMechanism of action of the new anti-ischemia drug ranolazine.Hypoxia. 4. Hypoxia and ion channel functionProtective effect of propranolol on mitochondrial function in the ischaemic heartAnti-anginal and anti-ischemic effects of late sodium current inhibitionExtracellular proton depression of peak and late Na⁺ current in the canine left ventricle.Extracellular proton modulation of the cardiac voltage-gated sodium channel, Nav1.5.Chronic heart failure slows late sodium current in human and canine ventricular myocytes: implications for repolarization variability.Filamin C: a novel component of the KCNE2 interactome during hypoxia.Na+ overload-induced mitochondrial damage in the ischemic heart.Acute hypoxia differentially regulates K(+) channels. Implications with respect to cardiac arrhythmia.Therapeutic potential for phenytoin: targeting Na(v)1.5 sodium channels to reduce migration and invasion in metastatic breast cancer.Reactive oxygen species in cardiac signalling: from mitochondria to plasma membrane ion channels.Voltage-gated sodium channels and metastatic disease.Contribution of protons to post-ischemic Na(+) and Ca(2+) overload and left ventricular mechanical dysfunction.The role of the persistent Na(+) current during cardiac ischemia and hypoxia.Late sodium current in failing heart: friend or foe?Inhibition of the late sodium current as a potential cardioprotective principle: effects of the late sodium current inhibitor ranolazine.Blockade of voltage-gated sodium channels inhibits invasion of endocrine-resistant breast cancer cellsModeling cardiac ischemiaRanolazine: a novel agent that improves dysfunctional sodium channels.
P2860
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P2860
Hypoxia increases persistent sodium current in rat ventricular myocytes.
description
1996 nî lūn-bûn
@nan
1996年の論文
@ja
1996年学术文章
@wuu
1996年学术文章
@zh-cn
1996年学术文章
@zh-hans
1996年学术文章
@zh-my
1996年学术文章
@zh-sg
1996年學術文章
@yue
1996年學術文章
@zh
1996年學術文章
@zh-hant
name
Hypoxia increases persistent sodium current in rat ventricular myocytes.
@en
Hypoxia increases persistent sodium current in rat ventricular myocytes.
@nl
type
label
Hypoxia increases persistent sodium current in rat ventricular myocytes.
@en
Hypoxia increases persistent sodium current in rat ventricular myocytes.
@nl
prefLabel
Hypoxia increases persistent sodium current in rat ventricular myocytes.
@en
Hypoxia increases persistent sodium current in rat ventricular myocytes.
@nl
P2093
P1476
Hypoxia increases persistent sodium current in rat ventricular myocytes.
@en
P2093
P304
P356
10.1113/JPHYSIOL.1996.SP021772
P407
P478
497 ( Pt 2)
P577
1996-12-01T00:00:00Z