Wnt signalling plays crucial roles in heart development, but is normally suppressed postnatally. In arrhythmogenic conditions, such as cardiac hypertrophy and heart failure, Wnt signalling is reactivated. To explore the potential role of Wnt signalling in arrhythmogenic electrical remodelling, we examined voltage‐dependent ion channels in cardiomyocytes. Treatment of neonatal rat ventricular myocytes with either recombinant Wnt3a protein or CHIR‐99021 (CHIR, a glycogen synthase kinase‐3β inhibitor) caused a dose‐dependent increase in Wnt target gene expression (Axin2 and Lef1), indicating activation of the Wnt/β‐catenin pathway. Cardiac Na⁺ current (I_Na) density was reduced by Wnt3a (−20 ± 4 vs. control −59 ± 7 pA pF⁻¹, at −30 mV) or CHIR (−22 ± 5 pA pF⁻¹), without changes in steady‐state activation, inactivation or repriming kinetics. Wnt3a and CHIR also produced dose‐dependent reductions in the mRNA level of Scn5a (the cardiac Na⁺ channel α subunit gene), as well as a 56% reduction (by Wnt3a) in the Na_v1.5 protein level. Consistent with I_Na reduction, action potentials in Wnt3a‐treated neonatal rat ventricular myocytes had a lower upstroke amplitude (91 ± 3 vs. control 137 ± 2 mV) and decreased maximum upstroke velocity (70 ± 10 vs. control 163 ± 15 V s⁻¹). In contrast, inward rectifier K⁺ current and L‐type Ca²⁺ channels were not affected by Wnt3a treatment. Taken together, our data indicate that the Wnt/β‐catenin pathway suppresses I_Na in postnatal cardiomyocytes and may contribute to ion channel remodelling in heart disease.