Hypertension in Cushing’s syndrome arises from complex mechanisms, including the activation of mineralocorticoid receptors when cortisol levels exceed the capacity of 11β-hydroxysteroid dehydrogenase type 2 to inactivate cortisol into cortisone, leading to sodium retention, potassium excretion and blood volume expansion, resulting in apparent mineralocorticoid excess and suppressed renin secretion. This evidence concerns the gene NR3C2 and Increased circulating aldosterone concentration.