Besides its central role in the regulation of extracellular fluid volume, aldosterone contributes to the development of cardiac pathologies such as hypertrophy. Moreover, aldosterone may also modulate cardiac electrophysiology, particularly the L-type Ca²⁺ current (I_CaL) and the transient outward K⁺ current (I_to). However, it is unknown whether a physiological increase in serum aldosterone concentration leads to alterations in ionic currents. In the present study we investigate the influence of low Na⁺ diet on cardiac electrophysiology in male Sprague-Dawley rats. Low Na⁺ diet (0.013% Na⁺, LSD) for 28 days increased serum aldosterone concentration from 0.19 ± 0.04 nM (n=6) in animals receiving control Na⁺ diet (0.3% Na⁺, CSD) to 16.1 ± 2.1 nM (n=6; p<0.0001) in animals on LSD. Femoral artery pressure was similar in both groups. Action potentials (AP) and ionic currents were assessed using the whole-cell patch-clamp technique. AP duration and I_to displayed the typical endocardial-to-epicardial gradient in magnitude but were not affected by LSD. I_CaL density was similar in myocytes isolated from CSD and LSD rats and averaged -12.9 ± 0.9 pApF^-1, n=18 and -13.7 ± 1.1 pApF^-1, n=16, respectively. Furthermore, LSD animals displayed normal surface ECGs. In summary, an increase in serum aldosterone concentration alone is not sufficient for a modulation of I_to and I_CaL densities in cardiac myocytes.