Late Na+ current produced by human cardiac Na+ channel isoform Nav1.5 is modulated by its β1 subunit
Author:
Publisher
Springer Science and Business Media LLC
Subject
Physiology
Link
http://link.springer.com/content/pdf/10.1007/s12576-009-0029-7.pdf
Reference53 articles.
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2. Maltsev VA, Undrovinas AI (2006) A multi-modal composition of the late Na+ current in human ventricular cardiomyocytes. Cardiovasc Res 69:116–127. doi: 10.1016/j.cardiores.2005.08.015
3. Maltsev VA, Silverman N, Sabbah HN, Undrovinas AI (2007) Chronic heart failure slows late sodium current in human and canine ventricular myocytes: implications for repolarization variability. Eur J Heart Fail 9:219–227. doi: 10.1016/j.ejheart.2006.08.007
4. Maltsev VA, Sabbah HN, Tanimura M, Lesch M, Goldstein S, Undrovinas AI (1998) Relationship between action potential, contraction-relaxation pattern, and intracellular Ca2+ transient in cardiomyocytes of dogs with chronic heart failure. Cell Mol Life Sci 54:597–605. doi: 10.1007/s000180050187
5. Undrovinas AI, Belardinelli L, Undrovinas NA, Sabbah HN (2006) Ranolazine improves abnormal repolarization and contraction in left ventricular myocytes of dogs with heart failure by inhibiting late sodium current. J Cardiovasc Electrophysiol 17:S169–S177. doi: 10.1111/j.1540-8167.2006.00401.x
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