Mineralocorticoid

Physiology and mechanism

Mineralocorticoids bind to mineralocorticoid receptors in target tissues, especially in renal distal tubules and collecting ducts. Their action increases sodium reabsorption and promotes excretion of potassium and hydrogen ions, mainly by modulating epithelial sodium channels and ion pumps. This regulation helps maintain electrolyte concentrations and extracellular fluid volume. Aldosterone secretion is tightly regulated by the renin–angiotensin–aldosterone system, serum potassium levels, and, to a lesser extent, ACTH.

Production and anatomy

These hormones are synthesized in the adrenal cortex, specifically the zona glomerulosa. Disorders of the adrenal cortex can lead to either excessive or deficient mineralocorticoid activity, with consequences for blood pressure and serum electrolytes. For basic context about the gland that produces them see the adrenal cortex entry: adrenal cortex.

Clinical importance and uses

• Excess activity (hyperaldosteronism) typically causes hypertension and low potassium.
• Deficiency may produce low blood pressure, elevated potassium and salt craving.
• Mineralocorticoid receptor antagonists are used to treat certain forms of heart failure and hypertension.
• Synthetic mineralocorticoids (for example, fludrocortisone) are used for replacement therapy in adrenal insufficiency.

Distinctions and notable facts

Mineralocorticoids are distinct from glucocorticoids, another corticosteroid subgroup more involved in metabolism and immune responses, though there is overlap and some hormones can bind both receptor types. Their name reflects their principal role in mineral (electrolyte) balance; for more on electrolyte physiology see electrolyte.