Evidence is increasing that aldosterone is not only regulating renal salt reabsorption but might also be a key player in the development of cardiomyopathies. Especially, chronically elevated levels of aldosterone (hyperaldosteronism) participate in the generation of atrial fibrillation, tachycardia, hypertrophy, fibrosis or inflammation. We elevated blood plasma levels of adult rats by implanting osmotic mini-pumps in 8 week old rats for 8 weeks (1,5 μg/h aldosterone). For the exploration on cellular excitation and contraction we performed isolation of ventricular and left and right atrial myocytes and studied cellular calcium handling, contractility and electrical properties of the cells.In ventricular myocytes we observed a severe drop-down of resting calcium, 1st amplitude (A1st) and steady-state amplitude (Astst) of global electrically induced calcium transients. For atrial myocytes of the right atrium such changes were rather pronounced while surprisingly, the left atrial myocytes displayed such effects to a much lesser degree. In line with changes in calcium handling contractility of the myocytes was also impaired. Here, right atrial myocytes displayed a pronounced negative contractility-frequency relationship (0.2 - 2 Hz) and their resting/diastolic sarcomer length was massively increased when compared to cells from control animals. When patch clamping the atrial myocytes we also found substantial changes in their action potentials (AP). Interestingly, for both left and right atrial cells, early phases of repolarisation were massively shortened (>50% change). Right atrial cells also showed a reduced AP rise time and their capacitance were significantly reduced (>30%).Here we demonstrate for the first time a differential effect of hyperaldosteronism on ventricular myocytes and cells from the left and right atrium.This work was supported by the DFG, BMBF and the Medical Faculty.