Late Na channels in cardiac cells: the physiological role of background Na channels.
Two types of the late Na channels, burst and background, were studied in Purkinje and ventricular cells. In the whole-cell configuration, steady-state Na currents were recorded at potentials (-70 to -80 mV) close to the normal cell resting potential. The question of the contribution of late Na channels to this background Na conductance was investigated. During depolarization, burst Na channels were active for periods (up to approximately 5 s), which exceeded the action potential duration. However, they eventually closed without reopening, indicating the presence of slow and complete inactivation. When, at the moment of burst channel opening, the potential was switched to -80 mV, the channel closed quickly without reopening. We conclude that the burst Na channels cannot contribute significantly to the background Na conductance. Background Na channels undergo incomplete inactivation. After a step depolarization, their activity decreased in time, approaching a steady-state level. Background Na channel openings could be recorded at constant potentials in the range from -120 to 0 mV. After step depolarizations to potentials near -70 mV and more negative, a significant fraction of Na current was carried by the background Na channels. Analysis of the background channel behavior revealed that their gating properties are qualitatively different from those of the early Na channels. We suggest that background Na channels represent a special type of Na channel that can play an important role in the initiation of cardiac action potential and in the TTX-sensitive background Na conductance.
Zilberter YuI
Department of Medicine (Cardiology), Duke University Medical Center, Durham, North Carolina 27710.
Starmer
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Starobin
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Grant
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D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002478:Cells, Cultured; D006321:Heart / Q000502:physiology*; D006352:Heart Ventricles; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D011690:Purkinje Fibers / Q000502:physiology*; D011817:Rabbits; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors
D015222:Sodium Channels; D013779:Tetrodotoxin