Mechanistic Links Between Na+ Channel (SCN5A) Mutations and Impaired Cardiac Pacemaking in Sick Sinus Syndrome
暂无分享,去创建一个
Henggui Zhang | Shin Inada | Ming Lei | J. Hancox | Henggui Zhang | O. Aslanidi | M. Boyett | S. Inada | T. Butters | M. Lei | Timothy D. Butters | Oleg V. Aslanidi | Mark R. Boyett | Jules C. Hancox
[1] Henggui Zhang,et al. Optimal velocity and safety of discontinuous conduction through the heterogeneous Purkinje-ventricular junction. , 2009, Biophysical journal.
[2] Yasutaka Kurata,et al. Regional difference in dynamical property of sinoatrial node pacemaking: role of na+ channel current. , 2008, Biophysical journal.
[3] J. Balser,et al. Enhanced Na(+) channel intermediate inactivation in Brugada syndrome. , 2000, Circulation research.
[4] A. Wilde,et al. A mutation in the human cardiac sodium channel (E161K) contributes to sick sinus syndrome, conduction disease and Brugada syndrome in two families. , 2005, Journal of molecular and cellular cardiology.
[5] A. Malliani,et al. Continuous 24-hour assessment of the neural regulation of systemic arterial pressure and RR variabilities in ambulant subjects. , 1990, Circulation.
[6] H Honjo,et al. Computer Three-Dimensional Reconstruction of the Sinoatrial Node , 2005, Circulation.
[7] Henggui Zhang,et al. Analysis of the Chronotropic Effect of Acetylcholine on Sinoatrial Node Cells , 2002, Journal of cardiovascular electrophysiology.
[8] L N Bouman,et al. Electrophysiology of the ageing rabbit and cat sinoatrial node--a comparative study. , 1993, European heart journal.
[9] M. Brignole,et al. Treatment of persistent sinus bradycardia with intermittent symptoms: are guidelines clear? , 2009, Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology.
[10] A. George,et al. Congenital sick sinus syndrome caused by recessive mutations in the cardiac sodium channel gene (SCN5A). , 2003, The Journal of clinical investigation.
[11] Henggui Zhang,et al. Atrial modulation of sinoatrial pacemaker rate , 1995 .
[12] M Lei,et al. Computational evaluation of the roles of Na+ current, iNa, and cell death in cardiac pacemaking and driving. , 2007, American journal of physiology. Heart and circulatory physiology.
[13] Colleen E Clancy,et al. Age-dependent changes in Na current magnitude and TTX-sensitivity in the canine sinoatrial node. , 2010, Journal of molecular and cellular cardiology.
[14] M R Boyett,et al. Correlation between electrical activity and the size of rabbit sino‐atrial node cells. , 1993, The Journal of physiology.
[15] Henggui Zhang,et al. SCN5A and sinoatrial node pacemaker function. , 2007, Cardiovascular research.
[16] A E Becker,et al. Functional and Morphological Organization of the Rabbit Sinus Node , 1980, Circulation research.
[17] N. Makita,et al. Enhanced sodium channel intermediate inactivation in Brugada syndrome , 2000 .
[18] W. Catterall,et al. Role of the C-terminal domain in inactivation of brain and cardiac sodium channels , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[19] D. Tester,et al. A novel C-terminal truncation SCN5A mutation from a patient with sick sinus syndrome, conduction disorder and ventricular tachycardia. , 2007, Cardiovascular research.
[20] P. C. Viswanathan,et al. Clinical, Genetic, and Biophysical Characterization of SCN5A Mutations Associated With Atrioventricular Conduction Block , 2002, Circulation.
[21] Henggui Zhang,et al. Mechanisms of transition from normal to reentrant electrical activity in a model of rabbit atrial tissue: interaction of tissue heterogeneity and anisotropy. , 2009, Biophysical journal.
[22] A. Yang,et al. Structural effects of an LQT-3 mutation on heart Na+ channel gating. , 2004, Biophysical journal.
[23] Y Rudy,et al. Ionic mechanisms of propagation in cardiac tissue. Roles of the sodium and L-type calcium currents during reduced excitability and decreased gap junction coupling. , 1997, Circulation research.
[24] C. Huang,et al. Genetic Na+ channelopathies and sinus node dysfunction. , 2008, Progress in biophysics and molecular biology.
[25] D. Severson,et al. Characteristics of nitric oxide‐mediated cholinergic modulation of calcium current in rabbit sino‐atrial node , 1998, The Journal of physiology.
[26] L. Crown,et al. Diagnosis and treatment of sick sinus syndrome. , 2003, American family physician.
[27] E. Lakatta,et al. Cholinergic receptor signaling modulates spontaneous firing of sinoatrial nodal cells via integrated effects on PKA-dependent Ca(2+) cycling and I(KACh). , 2009, American journal of physiology. Heart and circulatory physiology.
[28] H Zhang,et al. Mathematical models of action potentials in the periphery and center of the rabbit sinoatrial node. , 2000, American journal of physiology. Heart and circulatory physiology.
[29] H. Abriel,et al. Roles and regulation of the cardiac sodium channel Na v 1.5: recent insights from experimental studies. , 2007, Cardiovascular research.
[30] Robert H. Anderson,et al. New insights into pacemaker activity: promoting understanding of sick sinus syndrome. , 2007, Circulation.
[31] Robert H. Anderson,et al. New insights into Sick Sinus Syndrome , 2007 .
[32] D. Noble,et al. Requirement of neuronal‐ and cardiac‐type sodium channels for murine sinoatrial node pacemaking , 2004, The Journal of physiology.
[33] W. Baust,et al. The regulation of heart rate during sleep , 1969, Experimental Brain Research.
[34] G. Breithardt,et al. Pacemaker channel dysfunction in a patient with sinus node disease. , 2003, The Journal of clinical investigation.
[35] H. Brown,et al. Cardiac pacemaking in the sinoatrial node. , 1993, Physiological reviews.
[36] J. Lenfant,et al. Mechanism of muscarinic control of the high-threshold calcium current in rabbit sino-atrial node myocytes , 1993, Pflügers Archiv.