mineralocorticoider

Mineralocorticoiders, or mineralocorticoids, are a class of corticosteroid hormones produced by the adrenal cortex. The principal human mineralocorticoid is aldosterone; other steroids such as deoxycorticosterone can have mineralocorticoid activity in some settings. Synthetic mineralocorticoids, notably fludrocortisone, are used clinically to treat certain electrolyte and blood pressure disorders. Aldosterone is the dominant regulator of salt and fluid balance in the kidney.

Aldosterone production is localized to the zona glomerulosa of the adrenal cortex. Its release is mainly controlled by the renin-angiotensin-aldosterone system, with potassium level and, to a lesser extent, ACTH contributing. Hypovolemia, hyponatremia, or high potassium stimulate secretion; hypervolemia or high sodium suppress it.

Mechanism of action: Mineralocorticoids act by binding the mineralocorticoid receptor (MR) in epithelial cells of the distal nephron. Activated MR increases transcription of genes that raise ENaC activity and Na+/K+-ATPase expression, promoting sodium reabsorption and potassium excretion. The kidney expresses 11β-hydroxysteroid dehydrogenase type 2, which protects MR from cortisol.

Physiological role: By promoting sodium reabsorption, mineralocorticoids help regulate extracellular fluid volume, blood pressure, and acid-base balance. Their effects are interdependent with angiotensin II and vasopressin and vary by tissue context.

Clinical relevance: Excess mineralocorticoid activity causes hyperaldosteronism (hypertension with hypokalemia; primary forms include adenoma or hyperplasia; secondary forms arise from RAAS activation). Deficiency leads to hypoaldosteronism, contributing to hyperkalemia and acidosis in adrenal insufficiency. Treatments include MR antagonists such as spironolactone and eplerenone, and, for deficiency, replacement with fludrocortisone.