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Molecular dissection of cardiac repolarization by in vivo Kv4.3 gene transfer
Heart failure leads to marked suppression of the Ca(2+)-independent transient outward current (I(to1)), but it is not clear whether I(to1) downregulation suffices to explain the concomitant action potential prolongation. To investigate the role of I(to1) in cardiac repolarization while circumventing...
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| Autors principals: | , , |
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| Format: | Artigo |
| Idioma: | Inglês |
| Publicat: |
American Society for Clinical Investigation
2000
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| Matèries: | |
| Accés en línia: | https://ncbi.nlm.nih.gov/pmc/articles/PMC300832/ https://ncbi.nlm.nih.gov/pubmed/10772652 |
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