Late Na channels in cardiac cells: the physiological role of background Na channels - PubMed (original) (raw)
Comparative Study
Late Na channels in cardiac cells: the physiological role of background Na channels
Zilberter YuI et al. Biophys J. 1994 Jul.
Abstract
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.
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References
- J Gen Physiol. 1986 Feb;87(2):305-26 - PubMed
- J Gen Physiol. 1985 Nov;86(5):691-719 - PubMed
- Pflugers Arch. 1987 Jan;408(1):18-26 - PubMed
- Circ Res. 1987 Jun;60(6):897-913 - PubMed
- Jpn J Physiol. 1987;37(3):393-410 - PubMed
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