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• W1864296857 abstract "Key points Late Na + current ( I NaL ) contributes to action potential remodelling and Ca 2+ /Na + changes in heart failure. The molecular identity of I NaL remains unclear. The contributions of different Na + channel isoforms, apart from the cardiac isoform, remain unknown. We discovered and characterized a substantial contribution of neuronal isoform Na v 1.1 to I NaL . This new component is physiologically relevant to the control of action potential shape and duration, as well as to cell Ca 2+ dynamics, especially in heart failure. Abstract Late Na + current ( I NaL ) contributes to action potential (AP) duration and Ca 2+ handling in cardiac cells. Augmented I NaL was implicated in delayed repolarization and impaired Ca 2+ handling in heart failure (HF). We tested if Na + channel (Na v ) neuronal isoforms contribute to I NaL and Ca 2+ cycling defects in HF in 17 dogs in which HF was achieved via sequential coronary artery embolizations. Six normal dogs served as control. Transient Na + current ( I NaT ) and I NaL in left ventricular cardiomyocytes (VCMs) were recorded by patch clamp while Ca 2+ dynamics was monitored using Fluo‐4. Virally delivered short interfering RNA (siRNA) ensured Na v 1.1 and Na v 1.5 post‐transcriptional silencing. The expression of six Na v s was observed in failing VCMs as follows: Na v 1.5 (57.3%) > Na v 1.2 (15.3%) > Na v 1.1 (11.6%) > Na v 2.1 (10.7%) > Na v 1.3 (4.6%) > Na v 1.6 (0.5%). Failing VCMs showed up‐regulation of Na v 1.1 expression, but reduction of Na v 1.6 mRNA. A similar Na v expression pattern was found in samples from human hearts with ischaemic HF. VCMs with silenced Na v 1.5 exhibited residual I NaT and I NaL (∼30% of control) with rightwardly shifted steady‐state activation and inactivation. These currents were tetrodotoxin sensitive but resistant to MTSEA, a specific Na v 1.5 blocker. The amplitude of the tetrodotoxin‐sensitive I NaL was 0.1709 ± 0.0299 pA pF –1 ( n = 7 cells) and the decay time constant was τ = 790 ± 76 ms ( n = 5). This I NaL component was lacking in VCMs with a silenced Na v 1.1 gene, indicating that, among neuronal isoforms, Na v 1.1 provides the largest contribution to I NaL . At –10 mV this contribution is ∼60% of total I NaL . Our further experimental and in silico examinations showed that this new Na v 1.1 I NaL component contributes to Ca 2+ accumulation in failing VCMs and modulates AP shape and duration. In conclusion, we have discovered an Na v 1.1‐originated I NaL component in dog heart ventricular cells. This component is physiologically relevant to controlling AP shape and duration, as well as to cell Ca 2+ dynamics." @default.
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• W1864296857 date "2014-11-17" @default.
• W1864296857 modified "2023-10-16" @default.
• W1864296857 title "Contribution of sodium channel neuronal isoform Na_v1.1 to late sodium current in ventricular myocytes from failing hearts" @default.
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• W1864296857 doi "https://doi.org/10.1113/jphysiol.2014.278259" @default.
• W1864296857 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4376421" @default.
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