The mineralocorticoid receptor (MR) is involved in salt and water homeostasis and regulation of blood pressure but it can also independently elicit pathophysiological effects in the renocardiovascular system via an unknown mechanism. Both the MR and the closely related glucocorticoid receptor (GR) act as ligand-bound transcription factors at a common hormone response element. Nevertheless, they have different functions in the body and the reason for this is still unclear. One possible mechanism for pathophysiological MR effects and MR specificity is posttranscriptional regulation of genes, for example via modulation of miRNA expression. miRNAs are small RNAs that bind to the 3'UTR of certain mRNAs and lead to silencing or degradation of these mRNAs. To test this hypothesis, we determined the basal miRNA expression profile in cells relevant for pathophysiological MR effects, i.e. human aortic smooth muscle and endothelial cells. Next, we investigated whether activation of MR with its ligand aldosterone or activation of GR with dexamethasone leads to a change in these basal miRNA expression profiles. As a screening test we applied miRNA microarrays and subsequently validated our results with qPCR. Responses in both cell types were compared to differentiate between general and cell-type specific effects. In future we plan to test the MR- and GR- regulated miRNAs of our screening approach in more detail under more easily controllable conditions in HEK cells and we also plan to investigate possible targets of these miRNAs to gain insights into the mechanism of pathophysiological MR effects and MR specificity.