Aldosterone is a mineralocorticoid hormone responsible for regulation of sodium balance, potassium balance, extracellular fluid volume, blood pressure stability, and renal electrolyte handling. Its primary physiological action occurs in the distal nephron of the kidney, where it increases sodium reabsorption and potassium secretion through regulation of epithelial sodium channels and sodium-potassium ATPase transport systems.
By increasing sodium retention, aldosterone promotes water conservation and helps maintain circulating blood volume. The hormone also contributes to regulation of hydrogen ion secretion and acid-base balance. In addition to kidney effects, aldosterone acts within colon, sweat glands, salivary glands, vascular tissue, and cardiac tissue. Because electrolyte balance directly influences cellular excitability, vascular tone, and tissue hydration, aldosterone is essential for systemic fluid homeostasis.
Aldosterone is produced in the zona glomerulosa of the adrenal cortex from cholesterol through specialized steroidogenic enzyme pathways. Cholesterol undergoes conversion through multiple intermediates before aldosterone synthase, encoded by CYP11B2, catalyzes final synthetic steps unique to mineralocorticoid production.
Zona glomerulosa cells are highly specialized endocrine cells responsive to angiotensin II and extracellular potassium concentrations. Unlike cortisol-producing zona fasciculata tissue, mineralocorticoid-producing cells express distinct enzyme patterns allowing selective aldosterone synthesis. After production, aldosterone enters circulation and binds mineralocorticoid receptors in target tissues to regulate transcription of sodium-transport and potassium-transport proteins.
Aldosterone secretion is controlled mainly by the renin-angiotensin-aldosterone system and plasma potassium concentration. Reduced kidney perfusion, low sodium delivery to the macula densa, dehydration, or sympathetic nervous system activation increase renin release from juxtaglomerular cells. Renin leads to production of angiotensin II, which strongly stimulates zona glomerulosa aldosterone synthesis.
Elevated extracellular potassium directly depolarizes adrenal glomerulosa cells and stimulates aldosterone production independently of renin signaling. Natriuretic peptides, restoration of blood volume, and reduced angiotensin II suppress secretion. Aldosterone signaling activates mineralocorticoid receptors that increase expression of sodium channels, transport proteins, and ion-regulating enzymes. Through these integrated endocrine systems, aldosterone maintains extracellular fluid stability, electrolyte balance, vascular volume regulation, and long-term blood pressure homeostasis.
Aldosterone, via MR, drives renal sodium conservation and potassium excretion, stabilizing extracellular volume and acid–base balance.
