In human atrial fibrillation (AF), increased levels of reactive oxygen species, increased activity of the NADPH oxidase and increased expression of the small GTPase Rac1 have been reported. In a RacET transgenic mouse line, spontaneous AF occurs at ages >12 weeks. Here, we characterise atrial remodelling processes that take place in calcium handling and ion current. We used 4–6 months old male mice and age matched control mice. Echocardiography indicated mildly enlarged left atria while the right atria displayed several fold dilation. The analysis of whole cell calcium transients revealed that although both cell types displayed reduced calcium transient amplitudes, basal calcium concentration was significantly increased only in cells of the right atrium. Post-rest behaviour was unchanged. While in the left atrium (LA) caffeine responses were unchanged in amplitude but SERCA activity was down by almost 50%, cells from the right atrium (RA) showed significantly decreased caffeine signals (by 40%) and increased Na/Ca exchanger with an unchanged SERCA pump activity. Calcium sparks also displayed striking differences. While in RA their amplitude was reduced, recovery was slowed down and spatial spread was only slightly decreased (by 10%), cells from LA showed an increased amplitude (by 40%), faster recovery (up 20%) and a decreased spatial spread (down by >25 %). Action potentials recorded from LA and RA cells showed a slightly more negative resting membrane potentials in the myocytes from RacET with otherwise unchanged properties. From these data we conclude that Rac1 overexpression and the accompanying increased oxygene radical load results in atrial remodelling that is significantly different between the left and the right atrium. This work was supported by the DFG (SFB530, GraKo1320, KliFor196), the BfR and the BMBF.