A TTX-Sensitive Resting Na + Permeability Contributes to the Catecholaminergic Automatic Activity in Rat Pulmonary Vein
| Autor: | Malécot, Claire O., Bredeloux, Pierre, Findlay, Ian, Maupoil, Véronique |
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| Přispěvatelé: | Signalisation et Transports Ioniques Membranaires (STIM), Université de Poitiers-Université de Tours (UT)-Centre National de la Recherche Scientifique (CNRS), Université de Tours-Université de Poitiers-Centre National de la Recherche Scientifique (CNRS) |
| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
MESH: Rats
[SDV]Life Sciences [q-bio] MESH: Pulmonary Veins MESH: Myocytes Cardiac MESH: Rats Wistar TTX MESH: Tetrodotoxin MESH: Male MESH: Organ Culture Techniques MESH: Sodium Channels isolated cardiomyocytes MESH: Catecholamines MESH: Sodium MESH: Membrane Potentials atrial fibrillation MESH: Animals ranolazine MESH: Cell Membrane Permeability sodium channels quinidine |
| Zdroj: | Journal of Cardiovascular Electrophysiology Journal of Cardiovascular Electrophysiology, Wiley, 2015, 26 (3), pp.311-319. ⟨10.1111/jce.12572⟩ |
| ISSN: | 1045-3873 1540-8167 |
| DOI: | 10.1111/jce.12572⟩ |
| Popis: | International audience; Introduction: Ectopic activity arising from pulmonary veins (PV) plays a prominent role in the onset of atrial fibrillation in humans. Rat PV cardiac muscle cells have a lower resting membrane potential (RMP) than the left atria (LA) and presents in the presence of norepinephrine an automatic activity, which occurs in bursts. This study investigated the role of Na channels upon the RMP and the catecholaminergic automatic activity (CAA) in PV cardiac muscle.Methods and results: RMP and CAA experiments were performed in male Wistar rat PV. Whole-cell INa was recorded in isolated PV and LA cardiomyocytes. PV has a higher tetrodotoxin (TTX)-sensitive basal Na(+) permeability than the LA, due to a ∼ 5 mV more negative Na window current in the former tissue. TTX, quinidine, and ranolazine (1 to 10 μM each) decreased CAA incidence and arrhythmias by increasing burst intervals because of a reduction of the slope of slow depolarization between bursts. TTX and ranolazine also reduced burst duration. At 1 Hz, 10 μM quinidine, ranolazine, and TTX inhibited peak INa by 33%, 28%, and 98%, respectively. Each reduced the Na window current. There was no evidence for a TTX- or ranolazine-sensitive late Na current.Conclusion: Na channels confer a TTX-sensitive basal Na(+) permeability to rat PV cardiac muscle cells and contribute to the slope of slow depolarization between bursts of CAA. Na channel blockers act mostly via reduction of the Na window current. Ranolazine also has an anti-α1 adrenergic effect, which contributed to its antiarrhythmic effect. |
| Databáze: | OpenAIRE |
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