| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10953776 | Journal of Molecular and Cellular Cardiology | 2012 | 12 Pages |
Abstract
⺠INaL can disrupt cellular repolarization and increase propensity to ventricular arrhythmia. ⺠Although small compared to peak Na+ current, INaL increases Na+ loading in cardiac cells. ⺠Multiple cardiac pathological conditions share phenotypic manifestation of INaL upregulation. ⺠Specific pharmacological inhibition of INa is desired.
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Authors
Jonathan D. Moreno, Colleen E. Clancy,