NR3C2 and glucocorticoid-remediable aldosteronism: This is intriguing due to the notable rise in adrenocorticotropic hormone concentration during pregnancy, which directly regulates aldosterone production in familial hyperaldosteronism type I. To date, the improvement in BP in familial hyperaldosteronism type I during pregnancy has been attributed to elevated levels of progesterone, acting as a competitive antagonist of the mineralocorticoid receptor.