The cardiac sodium channel: Gating function and molecular pharmacology

Journal of Molecular and Cellular Cardiology

Volumn 33, Issue 4, 2001, Pages 599-613

  Balser, Jeffrey R ^a  

^a VANDERBILT UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Antiarrhythmic drugs; Brugada syndrome; Flecainide; Lidocaine; Long OT syndrome; Sodium channel

Indexed keywords

ANTIARRHYTHMIC AGENT; FLECAINIDE; LIDOCAINE; PHENYTOIN; SODIUM CHANNEL;

ARRHYTHMOGENESIS; BRUGADA SYNDROME; CHANNEL GATING; CONFERENCE PAPER; ELECTRIC FIELD; HEART ARRHYTHMIA; HEART ELECTROPHYSIOLOGY; HEART MUSCLE EXCITABILITY; HEART MUSCLE ISCHEMIA; HUMAN; LONG QT SYNDROME; PRIORITY JOURNAL; PROTEIN CONFORMATION; STRUCTURE ACTIVITY RELATION;

EID: 0034978313     PISSN: 00222828     EISSN: None     Source Type: Journal    
DOI: 10.1006/jmcc.2000.1346     Document Type: Conference Paper

References (127)

1. Mortality and morbidity in patients receiving encainide, flecainide, or placebo
2. + conduction and selectivity
3. Solution structure of the sodium channel inactivation gate
4. A quantitative description of membrane current and its application to conduction and excitation in nerve
5. Local anesthetics: Hydrophilic and hydrophobic pathways for the drug-receptor reaction
6. Time- and voltage-dependent interactions of the antiarrhythmic drugs with cardiac sodium channels
7. Structure and function of voltage-dependent sodium channels: Comparison of brain II and cardiac isoforms
8. Structure and function of voltage-gated sodium channels
9. From ionic currents to molecular mechanisms: The structure and function of voltage-gated sodium channels
10. Structure and function of the cardiac sodium channels
11. Expression of functional sodium channels from cloned cDNA
12. Primary structure and functional expression of the human cardiac tetrodotoxin-insensitive voltage-dependent sodium channel
13. Primary structure and functional expression of a mammalian skeletal muscle sodium channel
14. Structural parts involved in activation and inactivation of the sodium channel
15. Sodium channel activation gating is affected by substitutions of voltage sensor positive charges in all four domains
16. Sodium channel mutations in paramyotonia congenita uncouple inactivation from activation
17. Evidence for voltage-dependent S4 movement in sodium channels
18. + channel fast inactivation
19. Inactivation of the sodium channel. II. Gating current experiments
20. Fast and slow steps in the activation of sodium channels
21. A reinterpretation of mammalian sodium channel gating based on single channel recording
22. Sodium channels need not open before they inactivate
23. A revised view of cardiac sodium channel blockade in the long-QT syndrome
24. Inhibition of inactivation of single sodium channels by a site-directed antibody
25. Molecular basis of functional diversity of voltage-gated potassium channels in mammalian brain
26. +-channel inactivation
27. + channel inactivation gate during inactivation
28. Molecular analysis of the Na channel inactivation gate
29. A mutation in segment IVS6 disrupts fast inactivation of sodium channels
30. A critical role for transmembrane segment IVS6 of the sodium channel α subunit in fast inactivation
31. Interaction between the sodium channel inactivation linker and domain III S4-55
32. A critical role for the intracellular loop in domain IV of the sodium channel α subunit in fast inactivation
33. + channel probed by cysteine mutagenesis
34. Role of an S4-S5 linker in sodium channel inactivation probed by mutagenesis and a peptide blocker
35. Inactivation and secondary structure in the D4/S4-5 region of the SkM1 sodium channel
36. Glutamine substitution at alanine 1649 in the S4-S5 cytoplasmic loop of domain 4 removes the voltage sensitivity of fast inactivation in the human heart sodium channel
37. The role of the putative inactivation lid in sodium channel gating current immobilization
38. Slow inactivation of the sodium conductance in squid giant axons. Pronase resistance
39. Impaired slow inactivation in mutant sodium channels
40. Slow inactivation of sodium channels: More than just a laboratory curiosity
41. Slowly recovering cardiac sodium current in rat ventricular myocytes: Effects of conditioning duration and recovery potential
42. Two distinct congenital arrhythmias evoked by a multi-dysfunctional Na(+) channel
43. External pore residue mediates slow inactivation in μl rat skeletal muscle sodium channels
44. + channels is produced by a structural rearrangement of the outer vestibule
45. Structural determinants of slow inactivation in human cardiac and skeletal muscle sodium channels
46. Molecular dynamics of the sodium channel pore vary with gating: Interactions between P-segment motions and inactivation
47. Dynamic rearrangement of the outer mouth of a K channel during gating
48. Contribution of the selectivity filter to inactivation in potassium channels
49. Molecular motions within the pore of voltage-dependent sodium channels
50. + channel pores revealed by single- and double-cysteine replacements
51. 1 subunit with human cardiac (Hh1) and rat skeletal muscle (μl) sodium channel α subunits expressed in Xenopus oocytes
52. Ion channels as enzymes: Analogy or homology?
53. + channel's slow inactivation gate
54. Role of Domain 4 in sodium channel slow inactivation
55. Mechanistic link between local anesthetic action and inactivation gating probed by outer pore mutations in the rat μl sodium channel
56. SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndrome
57. Molecular mechanism for an inherited cardiac arrhythmia
58. + channel-linked long-QT syndrome
59. + channel mutations in the congenital long QT syndrome
60. A mutation (E1784K) in the carboxyl terminus of the cardiac Na channel causes autosomal dominant congenital long QT syndrome
61. Linking a genetic defect to its cellular phenotype in a cardiac arrhythmia
62. Sodium channel abnormalities are infrequent in patients with long QT syndrome: Identification of two novel SCN5A mutations
63. A de novo missense mutation of the SCN5A gene in long QT syndrome
64. Local anesthetics as effectors of allosteric gating: Lidocaine effects on inactivation-deficient rat skeletal muscle Na channels
65. Phenotypic characterization of a novel long QT syndrome mutation in the cardiac sodium channel
66. + channel exhibiting novel moleular mechanisms of long QT syndrome
67. + channel
68. + channel activity through interactions between alpha- and beta1-subunits
69. Arrhythmogenic mechanism of an LQT-3 mutation of the human heart Na(+) channel alpha-subunit: A computational analysis
70. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: A distinct clinical and electrocardiographic syndrome. A multicenter report
71. Sodium "channelopathies" and sudden death: Must you be so sensitive?
72. Genetic basis and molecular mechanism for idiopathic ventricular fibrillation
73. Electrophysiological characterization of SCN5A mutations causing long QT (E1784K) and Brugada (R1512W and R1432G) syndromes
74. Human SCN5A gene mutations alter cardiac sodium channel kinetics and are associated with the Brugada syndrome
75. Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent
76. SCN5A mutation (T1620M) causing Brugada syndrome exhibits different phenotypes when expressed in Xenopus oocytes and mammalian cells
77. Cardiac conduction defects associate with mutations in SCN5A
78. A single Na(+) channel mutation causing both long-QT and Brugada syndromes
79. Enhanced sodium channel intermediate inactivation in Brugada syndrome
80. Flecainide-induced arrhythmia in canine ventricular epicardium. Phase 2 rentry?
81. Sodium channel block produces opposite electrophysiological effects in canine ventricular epicardium and endocardium
82. "Brugada" syndrome: Clinical data and suggested pathophysiological mechanism
83. Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation
84. Differences in the electrophysiological response of canine ventricular epicardium and endocardium to ischemia: Role of the transient outward current
85. Electrophysiological properties and responses to simulated ischemia in cat ventricular myocytes of endocardial and epicardial origin
86. Reentrant arrhythmias in the subacute infarction period. The proarrhythmic effect of flecainide acetate on functional reentrant circuits
87. Actions of lidocaine on reentrant ventricular rhythms in the subacute myocardial infarction period in dogs
88. + currents in myocytes from epicardial border zone of the infarcted heart. A possible ionic mechanism for reduced excitability and postrepolarization refractoriness
89. + currents in ventricular myocytes from the epicardial border zone of the infarcted heart
90. Autonomic and antiarrhythmic drug modulation of ST segment elevation in patients with Brugada syndrome
91. ST segment elevation in the right precordial leads induced with class IC antiarrhythmic drugs: Insight into the mechanism of Brugada syndrome
92. Drug-induced J point elevation: A marker for genetic risk of sudden death or ECG curiosity?
93. Lidocaine block of cardiacsodium channels
94. Mechanisms of use-dependent block of sodium channels in excitable membranes by local anesthetics
95. + channels by local anesthetics
96. + channels
97. Point mutations at N434 in D1-S6 of mu1 Na(+) channels modulate binding affinity and stereoselectivity of local anesthetic enantiomers
98. + channels
99. +-channel activation gating
100. A molecular basis for the different local anesthetic affinities of resting versus open and inactivated states of the sodium channel
101. The inhibition of sodium currents in myelinated nerve by quaternary derivatives of lidocaine
102. Ultra-deep blockade of Na channels by a quaternary ammonium ion; catalysis by a transition-intermediate state?
103. Calcium channel characteristics conferred on the sodium channel by single mutations
104. Topology of the P segments in the sodium channel pore revealed by cysteine mutagenesis
105. Sodium channel selectivity filter regulates antiarrhythmic drug binding
106. Sodium channel block with mexilitine is effective in reducing dispersion of repolarization and preventing torsade de pointes in LQT2 and LQT3 models of the long-QT syndrome
107. Effects of flecainide in patients with new SCN5A mutation: Mutation-specific therapy for long-QT syndrome?
108. Lidocaine block of LQT-3 mutant human Na channels
109. + channel blockade and to increases in heart rate. Implications for gene-specific therapy
110. Pharmacological targeting of long QT mutant sodium channels
111. The elusive link between LQT3 and Brugada syndrome: The role of flecainide chellange
112. A molecular mechanism for class IA drug intolerance in the Brugada syndrome
113. Local anesthetic block of sodium channels in normal and pronase-treated squid axons
114. Sodium inactivation mechanism modulates qx-314 block of sodium channels
115. + channels
116. + channels
117. Kinetic effects of quaternary lidocaine block of cardiac sodium channels: A gating current study
118. Lidocaine alters activation gating of cardiac Na channels
119. Independent versus coupled inactivation in sodium channels. Role of the domain 2 S4 segment
120. Mechanism of frequency-dependent inhibition of sodium currents in the frog myelinated nerve by the lidocaine derivative gea 968
121. Molecular pharmacology of the sodium channel mutation D1790G linked to the long-QT syndrome
122. Functional consequences of lidocaine binding to slow-inactivated sodium channels
123. Lidocaine induces a slow inactivated state in rat skeletal muscle sodium channels
124. Isoform-specific lidocaine block of sodium channels explained by differences in gating
125. Inhibition of sodium currents in frog Ranvier node treated with local anesthetics: Role of slow sodium inactivation
126. pCa-sensitive slow inactivation and lidocaine-induced block of sodium channels in rat cardiac cells
127. A structural rearrangement in the sodium channel pore linked to slow inactivation and use dependence