Na+ currents are required for efficient excitation-contraction coupling in rabbit ventricular myocytes: a possible contribution of neuronal Na+ channels.
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Na⁺ transport in the normal and failing heart - remember the balanceAlterations in T-tubule and dyad structure in heart disease: challenges and opportunities for computational analysesNa+/Ca2+ exchange and Na+/K+-ATPase in the heartModeling effects of L-type ca(2+) current and na(+)-ca(2+) exchanger on ca(2+) trigger flux in rabbit myocytes with realistic T-tubule geometriesDecreased cardiac excitability secondary to reduction of sodium current may be a significant contributor to reduced contractility in a rat model of sepsis.Junctional cleft [Ca²⁺]i measurements using novel cleft-targeted Ca²⁺ sensorsDistinguishing between overdrive excited and suppressed ventricular beats in guinea pig ventricular myocardium.Neuronal Na+ channel blockade suppresses arrhythmogenic diastolic Ca2+ release.A null mutation of the neuronal sodium channel NaV1.6 disrupts action potential propagation and excitation-contraction coupling in the mouse heartThe interaction of Ca2+ with sarcomeric proteins: role in function and dysfunction of the heartNa+/Ca2+ exchanger-1 protects against systolic failure in the Akitains2 model of diabetic cardiomyopathy via a CXCR4/NF-κB pathway.Neuronal Na+ Channels Are Integral Components of Pro-arrhythmic Na+/Ca2+ Signaling Nanodomain That Promotes Cardiac Arrhythmias During β-adrenergic Stimulation.Localization of sodium channel subtypes in mouse ventricular myocytes using quantitative immunocytochemistry.Cardiac arrhythmia in a mouse model of sodium channel SCN8A epileptic encephalopathyCardiac sodium-calcium exchange and efficient excitation-contraction coupling: implications for heart disease.Dynamic local changes in sarcoplasmic reticulum calcium: physiological and pathophysiological roles.Microarchitecture of the dyad.Na/Ca exchange and contraction of the heart.Modeling calcium regulation of contraction, energetics, signaling, and transcription in the cardiac myocyte.Neuronal sodium channels: emerging components of the nano-machinery of cardiac calcium cycling.Species-Dependent Mechanisms of Cardiac Arrhythmia: A Cellular Focus.Modeling Na+-Ca2+ exchange in the heart: Allosteric activation, spatial localization, sparks and excitation-contraction coupling.Sensitized signalling between L-type Ca2+ channels and ryanodine receptors in the absence or inhibition of FKBP12.6 in cardiomyocytes.Cardiac Arrhythmias as Manifestations of Nanopathies: An Emerging ViewPharmacological characterization of crotamine effects on mice hind limb paralysis employing both ex vivo and in vivo assays: Insights into the involvement of voltage-gated ion channels in the crotamine action on skeletal muscles
P2860
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P2860
Na+ currents are required for efficient excitation-contraction coupling in rabbit ventricular myocytes: a possible contribution of neuronal Na+ channels.
description
2010 nî lūn-bûn
@nan
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
2010年论文
@zh
2010年论文
@zh-cn
name
Na+ currents are required for ...... tion of neuronal Na+ channels.
@en
Na+ currents are required for ...... tion of neuronal Na+ channels.
@nl
type
label
Na+ currents are required for ...... tion of neuronal Na+ channels.
@en
Na+ currents are required for ...... tion of neuronal Na+ channels.
@nl
prefLabel
Na+ currents are required for ...... tion of neuronal Na+ channels.
@en
Na+ currents are required for ...... tion of neuronal Na+ channels.
@nl
P2093
P1476
Na+ currents are required for ...... ution of neuronal Na+ channels
@en
P2093
John H B Bridge
Natalia S Torres
Robert Larbig
P304
P356
10.1113/JPHYSIOL.2010.194688
P407
P577
2010-11-01T00:00:00Z