Atrial fibrillation (AF) is the most common cardiac arrhythmias which leads to stroke. It is mediated by the activation of persistent Na channels (NaP) which in turn raises intracellular Ca2+ concentration ([Ca2+]i), a factor known to be associated with AF. Episodes of atrial arrhythmias, exhibit diurnal patterns suggesting a correlation between circadian rhythms and atrial electrophysiology. Circadian rhythms are mediated by cellular circadian clocks, made up of transcriptional-translational feedback loops consisting of several genes, in particular Bmal1. So far the correlation between the activated NaP channels and Bmal1 rhythmicity is unknown. The aim of this study is to assess the effects ATXII (Anemonia Sulcata toxin II, NaP channels opener) in the absence and presence of ranolazine (NaP channels blocker) on Bmal1 gene, driven by bioluminescence in cultured mouse atrial (HL-1-6) and embryonic fibroblast (MEF) cells. HL-1-6 were grown in Claycomb medium (10% FBS, 0.1 mM norepinephrine and 2 mM L-glutamine), whereas, MEFs were maintained in DMEM with 10% FBS. The cells were transfected with Bmal1::luciferase (BMAL1::LUC) probe to determine bioluminescence rhythmicity through long-term bioluminescence recording over several circadian cycles. Cells were serum shocked for 2 hrs in 50% FBS containing media to synchronise all cellular clocks. Cells were then incubated in control media alone or with 1nM ATXII in the absence/ presence of 10µM ranolazine throughout the duration of the experimental protocol. All data was expressed as mean ± S.E.M. Differences were deemed significant at P<0.05. Two-Way ANOVA was used to test significance between groups followed by Bonferroni post hoc comparison. Both HL-1-6 cells and MEFs exhibited 24 hrs circadian patterns of Bmal1 driven bioluminescence, under control conditions, with HL-1-6 cells exhibiting a period of 26.32 ± 1.76 hrs (n=8) and the later a period of 25.59±1.47 hrs (n=8). The circadian patterns in bioluminescence were highly disrupted in presence of ATXII in HL-1-6, with a 9 hrs shortening (17.28 ± 1.06 hrs; n=8; P<0.05) in their period, but not in MEFs which remained to show stable periods of 25.89 ± 2.1 hrs (n=8). The effect of ATXII on HL1-6 cells was reversed in presence of both ATXII and ranolazine (26.54 ± 1.67; n=8; P<0.05 vs ATXII). This study showed that in cultured atrial myocytes ATXII treatment leads to a significant shortening of Bmal1 driven bioluminescence by almost 9 hours, and such effect is fully reversed by ranolazine. Unlike MEFS where ATXII failed to affect Bmal1. In conclusion, this study suggests a possible correlation between ATXII induced atrial arrhythmias and Bmal1 gene and hence proposing a role for NaP channels in the disruption of atrial circadian rhythm.