The mineralocorticoid receptor binds cortisol as an active ligand, yet in normal people cortisol levels are not related to sodium retention. While in vitro the mineralocorticoid receptor has a similar affinity as aldosterone and cortisol, and in vivo cortisol is found in concentrations 100 to 1000 times higher than those of aldosterone, 11β-hydroxysteroid dehydrogenase 2 protects the mineralocorticoid receptor by reducing cortisol to cortisone, which is not an active ligand. This enzyme occurs in cells that contain the receptor. A similar enzyme is present in other tissues but works more slowly and backwards, converting cortisone to cortisol. Defects in this system can cause hypertension and can be diagnosed from the cortisol to cortisone ratio
Elevated cortisol:cortisone ratios may be found in chronic renal failure, excessive ingestion of glycyrrhetinic acid or derivatives, or in liver or bile-acid abnormalities.7 Even in these circumstances, however, determination of the cortisol:cortisone ratio is recommended to help shed light on the source of hypertension.
Useful for investigating suspected Cushing syndrome (hypercortisolism), Assisting in diagnosing acquired or inherited abnormalities of 11-beta-hydroxy steroid dehydrogenase (cortisol to cortisone ratio), and diagnosis of pseudo-hyperaldosteronism due to excessive licorice consumption