Figure 3.

The diagram shows a cortical collecting duct cell. The mineralocorticoid receptor (MR) has the same affinity for cortisol as for aldosterone (Aldo). The enzyme 11-β hydroxysteroid dehydrogenase (11-β HSD) “protects” the MR by metabolizing cortisol to cortisone, which has no affinity. A mutated or an inhibited enzyme results in an increased intracellular concentration of cortisol and an increased activation of the MR. A mutated MR can result in an altered configuration so that the MR is activated by sterols not containing a 21-hydroxyl group. Increased MR activity causes enhanced Na+ reabsorption (ENaC, Na-K-ATPase) and K+ excretion.