The functional properties of the sinus node (SN) and atrium are known to differ with gender: as compared to women, men have a lower extrinsic and intrinsic heart rate1 and a 1.5 fold higher chance of developing atrial fibrillation² (AF). To investigate the gender differences, we used quantitative PCR (qPCR) to compare ion channel gene expression in the SN and right atrium (RA) from young adult male (n=6) and female (n=6) Wistar Hannover rats. qPCR was carried out using an ABI 7900HT instrument with ABI Taqman probe assays to measure the relative abundance of 96 transcripts. In the SN, expression of the L-type Ca²⁺ channel Ca_v1.3 was 76% lower in the male (P < 0.05). In the RA, there were significant (P< 0.05) gender differences in 20% of the transcripts investigated, including Ca_vα2δ3 and Ca_vβ2 (accessory subunits for the L-type Ca²⁺ channel), K_v1.2 (contributes to I_to), K_v1.5 (responsible for I_K,ur) and K_vLQT1 (responsible for I_K,s). All differences between the male and female RA corresponded to lower expression in the male. There were more significant differences between the SN and RA in the male (51% of transcripts), than in the female (15% of transcripts). For example, in the male but not the female, Na_v1.1 (contributes to I_Na), Ca_v3.1 (contributes to I_Ca,T) and K_v1.5 were significantly more abundant in the SN, whereas Kir2.1(contributes to I_K,1) was significantly less abundant in the SN. Ca_v1.3 plays an important role in pacemaking in the SN, and a lower expression of this channel could possibly explain the lower intrinsic heart rate of the male. In AF, there is a reduction in the L-type Ca²⁺ current³, I_to and I_K,ur. Could a lower expression of Ca_vα2δ3, Ca_vβ2, K_v1.2 and K_v1.5 in the male RA contribute to the higher incidence of AF in men? The higher expression of K_vLQT1 in the female RA is surprising as gain of function mutations in K_vLQT1 have been linked with AF. The mRNA abundance for the intracellular Ca²⁺ handling proteins SERCA2a, NCX1 and IP3 Receptor Type I expression were significantly less abundant in the male RA. This again could have important implications for the function of the RA of the different genders. In addition, Ca_v1.3 and K_v1.5 protein was detected by western blotting, in both male and female SN and RA. In summary, our data show potentially important gender differences in ion channel expression in the SN and RA. The gender differences in ion channel gene expression in the RA could aid in understanding the mechanisms responsible for AF.