Aldosterone induces its effects by both genomic and non-genomic mechanisms. A pathophysiological influence of aldosterone on the cardiovascular system, which is induced by non-genomic signal paths, has been comparatively less well-researched than the effects on the heart of genomic mechanisms. In order to distinguish between these two effect-mechanisms of aldosterone, a variant of the human mineralocorticoid receptor (hMRDEF) in mice was cardiac-specifically over-expressed, which solely induces non-genomic effects. In organ bath investigations, contraction experiments on electrically stimulated left atria and frequency measurements on spontaneously beating right atria were carried out. A reduction of contraction strength (negatively inotropic) was shown, induced by aldosterone and activated via non-genomic signal paths. Furthermore, in transgenic mice an extended relaxation time of the left atria was shown under basal conditions and an extended P-wave in electrocardiograph (ECG) investigations.