Figure 1.

A schematic illustration of cortisol and cortisone molecular structures; cortisol can bind to mineralocorticoid receptor (MR) with the same affinity as aldosterone; the 11β-HSD2 enzyme converts cortisol in mineralocorticoid target tissues intos inactive cortisone preventing it from binding to MR. The intrinsic activity of 11β-HSD1 in peripheral tissues, especially in the liver and in adipose cells, may constitute the main determinant as far as the control of BP and the metabolic manifestations of cortisol excess are concerned.