Late Na channels in cardiac cells: the physiological role of background Na channels
- PMID: 7918982
- PMCID: PMC1225344
- DOI: 10.1016/S0006-3495(94)80464-3
Late Na channels in cardiac cells: the physiological role of background Na channels
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.
Similar articles
-
Gating of cardiac Na+ channels in excised membrane patches after modification by alpha-chymotrypsin.Biophys J. 1994 Jul;67(1):161-71. doi: 10.1016/S0006-3495(94)80465-5. Biophys J. 1994. PMID: 7918983 Free PMC article.
-
Cardiac Na currents and the inactivating, reopening, and waiting properties of single cardiac Na channels.J Gen Physiol. 1985 Nov;86(5):691-719. doi: 10.1085/jgp.86.5.691. J Gen Physiol. 1985. PMID: 2415670 Free PMC article.
-
Modification of sodium channel inactivation by alpha-chymotrypsin in canine cardiac Purkinje cells.J Cardiovasc Electrophysiol. 1993 Dec;4(6):686-94. doi: 10.1111/j.1540-8167.1993.tb01254.x. J Cardiovasc Electrophysiol. 1993. PMID: 8305988
-
The role of late I and antiarrhythmic drugs in EAD formation and termination in Purkinje fibers.J Cardiovasc Electrophysiol. 2006 May;17 Suppl 1:S71-S78. doi: 10.1111/j.1540-8167.2006.00386.x. J Cardiovasc Electrophysiol. 2006. PMID: 16686685 Review.
-
New studies of the excitatory sodium currents in heart muscle.Circ Res. 1985 Apr;56(4):475-85. doi: 10.1161/01.res.56.4.475. Circ Res. 1985. PMID: 2579746 Review.
Cited by
-
Tetrodotoxin-blockable calcium currents in rat ventricular myocytes; a third type of cardiac cell sodium current.J Physiol. 1997 Dec 1;505 ( Pt 2)(Pt 2):353-69. doi: 10.1111/j.1469-7793.1997.353bb.x. J Physiol. 1997. PMID: 9423179 Free PMC article.
-
Pathophysiology of the cardiac late Na current and its potential as a drug target.J Mol Cell Cardiol. 2012 Mar;52(3):608-19. doi: 10.1016/j.yjmcc.2011.12.003. Epub 2011 Dec 16. J Mol Cell Cardiol. 2012. PMID: 22198344 Free PMC article. Review.
-
Chronic heart failure slows late sodium current in human and canine ventricular myocytes: implications for repolarization variability.Eur J Heart Fail. 2007 Mar;9(3):219-27. doi: 10.1016/j.ejheart.2006.08.007. Epub 2006 Oct 24. Eur J Heart Fail. 2007. PMID: 17067855 Free PMC article.
-
The arrhythmogenic consequences of increasing late INa in the cardiomyocyte.Cardiovasc Res. 2013 Sep 1;99(4):600-11. doi: 10.1093/cvr/cvt145. Epub 2013 Jun 10. Cardiovasc Res. 2013. PMID: 23752976 Free PMC article. Review.
-
I(Ca(TTX)) channels are distinct from those generating the classical cardiac Na(+) current.Biophys J. 2001 Nov;81(5):2647-59. doi: 10.1016/s0006-3495(01)75908-5. Biophys J. 2001. PMID: 11606278 Free PMC article.
References
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources