Mathematical Model of the Rapidly Activating Delayed Rectifier Potassium Current IKr in Rabbit Sinoatrial Node
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[1] R. Wilders,et al. Atrio-Sinus Interaction Demonstrated by Blockade of the Rapid Delayed Rectifier Current , 2002, Circulation.
[2] D. Noble,et al. A model of sino-atrial node electrical activity based on a modification of the DiFrancesco-Noble (1984) equations , 1984, Proceedings of the Royal Society of London. Series B. Biological Sciences.
[3] Gary Yellen,et al. The inward rectification mechanism of the HERG cardiac potassium channel , 1996, Nature.
[4] W H Lamers,et al. Distribution of atrial and nodal cells within the rabbit sinoatrial node: models of sinoatrial transition. , 1998, Circulation.
[5] H. Strauss,et al. Time, voltage and ionic concentration dependence of rectification of h‐erg expressed in Xenopus oocytes , 1996, FEBS letters.
[6] C. Nichols,et al. Inward rectifiers in the heart: an update on I(K1). , 2001, Journal of molecular and cellular cardiology.
[7] Antonio Zaza,et al. Ionic currents during sustained pacemaker activity in rabbit sino‐atrial myocytes , 1997, The Journal of physiology.
[8] Harry J. Witchel,et al. Time course and voltage dependence of expressed HERG current compared with native ”rapid” delayed rectifier K current during the cardiac ventricular action potential , 1998, Pflügers Archiv.
[9] H. Brown,et al. Cardiac pacemaking in the sinoatrial node. , 1993, Physiological reviews.
[10] 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.
[11] J W Clark,et al. A mathematical model of primary pacemaking cell in SA node of the heart. , 1982, The American journal of physiology.
[12] N Lovell,et al. Ion currents underlying sinoatrial node pacemaker activity: a new single cell mathematical model. , 1996, Journal of theoretical biology.
[13] A. Brown,et al. Pathways of HERG inactivation. , 1999, American journal of physiology. Heart and circulatory physiology.
[14] O Gryshchenko,et al. Ischemia alters the electrical activity of pacemaker cells isolated from the rabbit sinoatrial node. , 2002, American journal of physiology. Heart and circulatory physiology.
[15] H. Strauss,et al. Activation and inactivation kinetics of an E-4031-sensitive current from single ferret atrial myocytes. , 1996, Biophysical journal.
[16] Akinori Noma,et al. Pacemaker Mechanisms of Rabbit Sinoatrial Node Cells , 1982 .
[17] G. Robertson,et al. HERG, a human inward rectifier in the voltage-gated potassium channel family. , 1995, Science.
[18] Anthony Varghese,et al. Effects of premature stimulation on HERG K+ channels , 2001, The Journal of physiology.
[19] M. Vassalle,et al. Role of dual pacemaker mechanisms in sinoatrial node discharge. , 2000, Journal of biomedical science.
[20] J. Boineau,et al. Morphological and membrane characteristics of spider and spindle cells isolated from rabbit sinus node. , 2001, American journal of physiology. Heart and circulatory physiology.
[21] W. Trautwein,et al. Calcium currents in single SA nodal cells of the rabbit heart studied with action potential clamp , 1989, Pflügers Archiv - European Journal of Physiology.
[22] A E Becker,et al. Functional and Morphological Organization of the Rabbit Sinus Node , 1980, Circulation research.
[23] M. Sanguinetti,et al. Fast inactivation causes rectification of the IKr channel , 1996, The Journal of general physiology.
[24] A. Noma,et al. Reconstruction of sino-atrial node pacemaker potential based on the voltage clamp experiments. , 1980, The Japanese journal of physiology.
[25] K. Ono,et al. Role of rapidly activating delayed rectifier K+ current in sinoatrial node pacemaker activity. , 1995, The American journal of physiology.
[26] D M Roden,et al. Rapid inactivation determines the rectification and [K+]o dependence of the rapid component of the delayed rectifier K+ current in cardiac cells. , 1997, Circulation research.
[27] R Wilders,et al. Pacemaker activity of the rabbit sinoatrial node. A comparison of mathematical models. , 1991, Biophysical journal.
[28] H Honjo,et al. The sinoatrial node, a heterogeneous pacemaker structure. , 2000, Cardiovascular research.
[29] John W. Clark,et al. Parasympathetic modulation of sinoatrial node pacemaker activity in rabbit heart: a unifying model. , 1999, American journal of physiology. Heart and circulatory physiology.
[30] Itsuo Kodama,et al. Heterogeneity of 4-aminopyridine-sensitive current in rabbit sinoatrial node cells. , 1999, American journal of physiology. Heart and circulatory physiology.
[31] Jeffrey R. Balser,et al. A sensitive mechanism for cation modulation of potassium current , 2000, Nature Neuroscience.
[32] N. Hagiwara,et al. Contribution of two types of calcium currents to the pacemaker potentials of rabbit sino‐atrial node cells. , 1988, The Journal of physiology.
[33] H Honjo,et al. Characterisation of the transient outward K+ current in rabbit sinoatrial node cells. , 2000, Cardiovascular research.
[34] M. Sanguinetti,et al. A mechanistic link between an inherited and an acquird cardiac arrthytmia: HERG encodes the IKr potassium channel , 1995, Cell.
[35] W. Giles,et al. Effect of hydrogen peroxide on the membrane currents of sinoatrial node cells from rabbit heart. , 2000, American journal of physiology. Heart and circulatory physiology.
[36] H. Kasanuki,et al. Properties of the transient outward current in rabbit sino-atrial node cells. , 1999, Journal of molecular and cellular cardiology.
[37] H. Strauss,et al. A quantitative analysis of the activation and inactivation kinetics of HERG expressed in Xenopus oocytes , 1997, The Journal of physiology.
[38] M. Sanguinetti,et al. Molecular biology of K(+) channels and their role in cardiac arrhythmias. , 2001, The American journal of medicine.
[39] R. Kumar,et al. Electrical interactions between a rabbit atrial cell and a nodal cell model. , 1998, American journal of physiology. Heart and circulatory physiology.
[40] F. Conti,et al. The steady-state properties of an ion exchange membrane with mobile sites. , 1966, Biophysical journal.
[41] M Lei,et al. Two components of the delayed rectifier potassium current, IK, in rabbit sino‐atrial node cells , 1996, Experimental physiology.
[42] T. C. West,et al. Interactions of K, Na, and vagal stimulation in the S-A node of the rabbit. , 1967, The American journal of physiology.
[43] H. Jongsma,et al. Spatial distribution of connexin43, the major cardiac gap junction protein, visualizes the cellular network for impulse propagation from sinoatrial node to atrium. , 1995, Circulation research.
[44] B. Fermini,et al. Removal of sialic acid alters both T- and L-type calcium currents in cardiac myocytes. , 1991, The American journal of physiology.
[45] J. Clark,et al. A mathematical model of a rabbit sinoatrial node cell. , 1994, The American journal of physiology.
[46] R Wilders,et al. Spatial and functional relationship between myocytes and fibroblasts in the rabbit sinoatrial node. , 1992, Journal of molecular and cellular cardiology.
[47] S. Heinemann,et al. Molecular determinants for activation and inactivation of HERG, a human inward rectifier potassium channel. , 1996, The Journal of physiology.
[48] A. Hodgkin,et al. A quantitative description of membrane current and its application to conduction and excitation in nerve , 1952, The Journal of physiology.
[49] T. Shibasaki,et al. Conductance and kinetics of delayed rectifier potassium channels in nodal cells of the rabbit heart. , 1987, The Journal of physiology.
[50] J. Hancox,et al. An investigation of the role played by the E-4031-sensitive (rapid delayed rectifier) potassium current in isolated rabbit atrioventricular nodal and ventricular myocytes , 1999, Pflügers Archiv.