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Title:DEVELOPMENT OF A DYNAMIC GAP JUNCTION MODEL INCLUDING THE Ca2+ GATE
DOI No:10.1142/9789812702234_0018
Source:ADVANCES IN ELECTROCARDIOLOGY 2004 (pp 75-80)
Author(s):CHIAKI OKA
Cell / Biodynamic Simulation Project, Kyoto University, Department of Physiology and Biophysics, Kyoto University Graduate School of Medicine, Yoshidakonoe-cho, Sakyo-ku, Kyoto 606-8501, Japan

HIROYUKI MATSUDA
Cell / Biodynamic Simulation Project, Kyoto University, Department of Physiology and Biophysics, Kyoto University Graduate School of Medicine, Yoshidakonoe-cho, Sakyo-ku, Kyoto 606-8501, Japan

NOBUAKI SARAI
Cell / Biodynamic Simulation Project, Kyoto University, Department of Physiology and Biophysics, Kyoto University Graduate School of Medicine, Yoshidakonoe-cho, Sakyo-ku, Kyoto 606-8501, Japan

SATOSHI MATSUOKA
Cell / Biodynamic Simulation Project, Kyoto University, Department of Physiology and Biophysics, Kyoto University Graduate School of Medicine, Yoshidakonoe-cho, Sakyo-ku, Kyoto 606-8501, Japan

AKINORI NOMA
Cell / Biodynamic Simulation Project, Kyoto University, Department of Physiology and Biophysics, Kyoto University Graduate School of Medicine, Yoshidakonoe-cho, Sakyo-ku, Kyoto 606-8501, Japan

Abstract:The dynamic range of the [Ca2+]-conductance relationship of the gap junction channel overlaps with the concentration range of the Ca2+ transient during a twitch contraction. However, this chemical gating of gap junctions has never been included in models examining conduction of cardiac excitation. Based on published data, we tentatively assumed a variety of time constants for the Ca2+ gate, and implemented the Ca2+ gate into the cardiac cell model. When the Ca2+-overload was induced by inhibiting Na+,K+ - ATPase in a paired cell model, the propagation of the action potential in a partner cell was more delayed as the time constant of the Ca2+ gate was decreased. We conclude that the Ca2+ gate of the gap junction channel is essential in determining the propagation of the action potential.
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