We have previously shown that in rats ascending aortic stenosis (AS) within one week leads to cardiac hypertrophy, a reduction in the transient outward K⁺ current (I_to) and an increase in action potential duration (APD). Here we investigate the effects of the antioxidant n-acetylcysteine (NAC) on the cellular cardiac electrophysiology of female Sprague Dawley rats with AS. Rats were treated with NAC (10 g/l in drinking water) or control solution one week before the intervention and in the week following AS. Seven days post AS, blood pressure and left ventricular pressure were measured, before the heart was excised. Single cells were isolated from endocardial and epicardial layers of the left ventricular free wall and investigated using the ruptured-patch configuration of the whole-cell patch-clamp technique. Systolic blood pressure (NAC: 943 mmHg, n=6, control: 10411 mmHg, n=5) and left ventricular peak pressure (NAC: 1547 mmHg, n=6, control: 16811 mmHg, n=5) were not significantly altered in the NAC group. Cell capacity as index of cell size was markedly reduced in myocytes isolated from NAC animals (141.03.8pF, n=71 vs. 161.84.1pF, n=75, p<0.001). APD90 was similar in both groups (NAC: epicardial: 85.620.4ms, n=27, endocardial: 303.750.6ms, n=19; control: epicardial: 114.927.2ms, n=22, endocardial: 338.035.0ms, n=19). While I_to was not significantly altered by NAC treatment, the density of the L-type Ca²⁺ current (I_CaL) was 26% decreased in the NAC group (12.51.1pApF-1, n=18 vs. 16.91.0pApF 1, n=28, p<0.01, endocardial and epicardial cells pooled). We conclude that NAC treatment ameliorates cellular hypertrophy and reduces the density of I_CaL in rats with AS.