Cortisol in concentrations within the therapeutic range inhibits calcium response of fibroblast to angiotensin II. In physiological concentrations, cortisol potentiates the effects of angiotensin II via modulation of membrane mineralocorticoid receptors. The inhibitory effects of glucocorticoids on cell proliferation and collagen synthesis are manifestations of its genomic effects mediated by intracellular receptors. The use of glucocorticoid preparation based on nanosized polymer structure made it possible to distinguish between the genomic and nongenomic mechanisms of regulation of activity of target-cells.