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Mineralocorticoids

Mineralocorticoida

For medical students2 min readUpdated 2026-10-10

Mineralocorticoids are a group of steroid hormones and drugs that regulate the body's water and electrolyte balance. The main endogenous representative is aldosterone, alongside synthetic agents such as desoxycortone acetate and fludrocortisone.

Main targetDistal convoluted tubules and collecting ducts of the kidneys

DrugsDesoxycortone acetate, fludrocortisone

Main effectEnhanced sodium reabsorption and potassium excretion

Half-lifeAldosterone — 15–20 minutes, desoxycortone — 70 minutes

General Characteristics and Regulation

The endogenous precursors and hormones in this group are aldosterone (the primary mineralocorticoid) and desoxycortone. Their secretion is regulated by adrenocorticotropic hormone (ACTH).

Under normal salt intake, the daily secretion of aldosterone is 100–200 mcg, and desoxycortone is about 200 mcg. These hormones have a short half-life: aldosterone is cleared in 15–20 minutes, and desoxycortone in 70 minutes. Aldosterone is transported bound to plasma proteins. The majority of metabolites are excreted by the kidneys: 70% as conjugates (tetrahydroaldosterone) and 30% in free form or as 3-oxoglucuronide.

Mechanism of Action and Physiological Effects

The molecular mechanism is based on binding to specific mineralocorticoid receptors located in the cytoplasm of target cells.

Primary sites of action: Kidneys (late distal tubules and cortical collecting ducts).
Extrarenal targets: Sweat and salivary glands, as well as the gastrointestinal mucosa.

The main pharmacodynamic effect is the stimulation of sodium ion (Na+) reabsorption and the enhancement of potassium ion (K+) excretion.

Pharmacology of Desoxycortone Acetate

Desoxycortone acetate is a synthetic analogue. Its pharmacological features include:

Mechanism: Stimulates the synthesis of sodium transporter proteins.
Selectivity: The drug has virtually no effect on carbohydrate metabolism (lacks significant glucocorticoid activity) and does not affect pigmentation, estrogenic, or androgenic functions.
Indications: Acute and chronic adrenocortical insufficiency, generalized muscle weakness (myasthenia gravis).
Contraindications: Congestive heart failure, arterial hypertension, atherosclerosis, and severe hepatic or renal disease.

Characteristics of Fludrocortisone and Dose-Dependency

Fludrocortisone is a potent steroid with a mixed activity profile, combining both mineralocorticoid and glucocorticoid properties.

Its effects depend on the administered dose:

Low doses (0.1 mg 2–7 times a week) exhibit pronounced mineralocorticoid activity.
High doses trigger glucocorticoid properties.

The drug is the most widely used mineralocorticoid and serves as a sodium-retaining agent, primarily for chronic adrenocortical insufficiency in combination with hydrocortisone.

Mnemonic

MineraLO- Natrium Kalium: Mineralocorticoids retain Natrium (sodium in) and excrete Kalium (potassium out).

Frequently asked questions

What factors and systems physiologically regulate aldosterone secretion?

Aldosterone secretion is regulated by adrenocorticotropic hormone. When circulating blood volume drops—such as during hemorrhage, vomiting, or diarrhea—the renin-angiotensin-aldosterone system is activated, leading to secondary aldosteronism.

What side effects can occur with prolonged use of mineralocorticoids?

Prolonged use of mineralocorticoids leads to fluid and electrolyte disturbances associated with excessive sodium retention and potassium loss.

Water and sodium retention — leads to marked edema and the onset or exacerbation of arterial hypertension.
Hypokalemia — causes generalized muscle weakness and various cardiac arrhythmias.

How do mineralocorticoids affect the acid-base balance of the blood?

Mineralocorticoids promote metabolic (excretory) alkalosis due to alterations in electrolyte balance.

Hydrogen ion excretion — the hormones directly enhance renal excretion of hydrogen and ammonium ions.
Hypokalemia — increased potassium excretion lowers blood potassium levels, which drives proton influx into cells and increases proton secretion into the tubular lumen.
Sodium retention — aldosterone enhances sodium reabsorption in renal tubules, further aggravating alkalosis.

Which gland regulates mineralocorticoid secretion?

Mineralocorticoid secretion is regulated by adrenocorticotropic hormone (ACTH).

What are the main extrarenal targets of mineralocorticoids?

Extrarenal targets include sweat and salivary glands, as well as the gastrointestinal mucosa.

What is the specific nature of fludrocortisone's action based on dosage?

At low doses, the drug exhibits pure mineralocorticoid activity, whereas at high doses, its glucocorticoid properties become active.

Go deeper

Pharmacokinetics and metabolism of aldosterone in the liver and kidneys
Role of sodium transport proteins in distal tubule epithelial cells
Clinical manifestations of hyperaldosteronism and hypoaldosteronism
Interaction of fludrocortisone and hydrocortisone in replacement therapy
Mineralocorticoid receptor antagonists and steroid synthesis inhibitors