mineralocorticoids

Mineralocorticoids are a class of steroid hormones that regulate electrolyte and water balance in the body. In humans, the principal mineralocorticoid is aldosterone, produced by the adrenal cortex’s zona glomerulosa. Aldosterone acts on mineralocorticoid receptors in principal cells of the kidney’s distal nephron, as well as in the colon and sweat glands, to increase sodium reabsorption and potassium excretion, with secondary effects on water retention and acid–base balance.

The effects of aldosterone are mediated mainly by genomic mechanisms that upregulate the transcription of proteins such as the epithelial sodium channel (ENaC), the Na+/K+-ATPase pump, and the serine/threonine kinase SGK1, enhancing sodium reabsorption and potassium secretion. Rapid, non-genomic actions on ion channels can also occur. Aldosterone activity is tightly regulated by the renin–angiotensin–aldosterone system (RAAS); low blood pressure or low sodium stimulates renin release and angiotensin II, which in turn increases aldosterone secretion. Potassium level and adrenocorticotropic hormone (ACTH) provide additional regulatory input.

Clinically, disorders of mineralocorticoids include hyperaldosteronism, causing hypertension and hypokalemia, and hypoaldosteronism, leading to hyperkalemia and salt-wasting. Primary hyperaldosteronism (e.g., Conn’s syndrome) arises from autonomous aldosterone production, whereas secondary forms result from RAAS activation due to heart failure, liver cirrhosis, or nephrotic syndrome. Treatments include mineralocorticoid receptor antagonists such as spironolactone and eplerenone, or mineralocorticoid replacement with fludrocortisone in adrenal insufficiency. In aldosterone-sensitive tissues, 11β-hydroxysteroid dehydrogenase type 2 protects the receptor from cortisol, which otherwise has mineralocorticoid activity.