The mineralocorticoid receptor (MR) is an aldosterone-dependent transcription factor that physiologically regulates blood pressure but can also lead to inflammation, hypertrophy, fibrosis and endothelial dysfunctions in the cardiovascular system. Several studies indicate that a parainflammatory micro-milieu with oxidative and nitrosative stress represents a possible trigger to induce pathophysiological MR effects. During ageing or cardiovascular diseases, vascular cells are increasingly exposed to such a parainflammatory micro-milieu. We hypothesise that this leads to changes in the aldosterone-induced posttranslational modification (PTM) pattern of MR or associated proteins, resulting in an inadequately high MR activation and consequently leading to pathophysiological MR effects. The focus of our investigations is to explore the influence of nitrosative stress, especially nitric oxide (NO) and peroxynitrite (ONOO-), on the PTM pattern of the MR and on MR signalling and function.