Lesson 9: Hormones and Regulation: Adrenal glands: Mineralocorticoids

What is the primary mineralocorticoid produced in the adrenal cortex?

Aldosterone.

What type of hormone is aldosterone?

A steroid hormone (lipophilic).

How does aldosterone circulate in blood?

Mostly bound to proteins, some free.

What are the main homeostatic functions of aldosterone?

Regulates Na+, K+, H+ balance; water homeostasis; blood volume and blood pressure; pH balance.

What is the correct sequence from renin release to aldosterone secretion?

Angiotensinogen → Angiotensin I → Angiotensin II → Aldosterone.

Where is angiotensinogen produced and how does it circulate?

Produced by the liver; small peptide that circulates continuously in blood.

What are the main stimuli for renin-angiotensin-aldosterone system activation?

Hypotension, hyperkalemia, hyponatremia, increased sympathetic activation.

Which two stimuli are the most important for aldosterone release?

Hypotension (low BP/low Na+) and hyperkalemia.

What detects low BP or sodium to trigger renin release?

Juxtaglomerular apparatus in the kidney.

What enzyme converts angiotensin I to angiotensin II?

ACE (angiotensin converting enzyme), mainly in lung capillaries.

What is the direct effect of angiotensin II on the adrenal gland?

Stimulates aldosterone secretion from zona glomerulosa.

Beyond stimulating aldosterone, what is a key direct action of angiotensin II on vessels?

Peripheral vasoconstriction → raises systemic blood pressure.

How does hyperkalemia directly affect the adrenal gland?

Directly stimulates aldosterone secretion.

What are the main target tissues of aldosterone?

Epithelial cells in distal tubules and collecting ducts of nephron (also salivary glands, sweat glands, gastric mucosa, large intestine).

What is the primary site of aldosterone action in the nephron?

Distal convoluted tubule and collecting duct.

What receptor does aldosterone bind to?

Mineralocorticoid receptor (MR) in the cytoplasm.

What effect does aldosterone have on sodium transport in the nephron?

↑ Na+ channels (apical) and ↑ Na+/K+ pumps (basolateral) → sodium reabsorption.

What anion follows sodium reabsorption in distal nephron under aldosterone?

Chloride (Cl-) follows Na+ to maintain electroneutrality; water follows osmotically.

What happens to water when sodium is reabsorbed under aldosterone influence?

Water follows sodium → increases blood volume and blood pressure.

What effect does aldosterone have on potassium?

Enhances K+ secretion via apical K+ channels → lowers plasma K+.

What effect does aldosterone have on hydrogen ions?

Enhances H+ secretion via apical pumps → helps control plasma pH.

What is the quick summary of aldosterone's kidney actions on membranes?

↑ ENaC (apical Na+ channels), ↑ Na+/K+ ATPase (basolateral), ↑ apical K+ channels, ↑ apical H+ pumps.

What are the general effects of aldosterone?

Na+ and water retention (↑ BP/volume), K+ excretion (protects against hyperkalemia), H+ excretion (helps correct acidosis).

In Addison's disease, which adrenal hormones are deficient?

Both cortisol (glucocorticoid) and aldosterone (mineralocorticoid).

In Addison's disease, which deficiency tends to appear first?

Glucocorticoid deficiency appears first, then mineralocorticoid deficiency follows.

Why can early glucocorticoid deficiency be partially "masked" in Addison's?

Mineralocorticoids can engage overlapping receptor pathways, partially masking early GC deficiency signs.

What is the underlying pathology of Addison's disease?

Degeneration of adrenal cortex (90% loss), medulla intact.

Why is Addison's disease called the "Great Pretender"?

Clinical signs are vague and mimic many other conditions.

What are the key signs of cortisol deficiency in Addison's disease?

Poor stress response, weakness, hypoglycemia, lethargy.

What are the key signs of aldosterone deficiency in Addison's disease?

Sodium/water loss → dehydration, hypovolemia; K+/H+ retention → hyperkalemia, metabolic acidosis; bradycardia; ECG changes.

What is the therapeutic goal in Addison's disease?

Replace missing glucocorticoids and mineralocorticoids; treat hypoglycemia; fluid therapy; nutritional support; emergency care in Addisonian crisis.

What clinical scenario suggests hyperaldosteronism in cats?

Hypertension, muscle weakness, hypokalemia, ± polydipsia/polyuria; often due to unilateral adrenocortical tumor.

How does aldosterone excess cause hypertension?

Continuous Na+ and water retention → hypervolemia → ↑ systemic arterial pressure.

How does aldosterone excess cause muscle weakness?

K+ loss → hypokalemia → impaired muscle function and excitability.

What are the biochemical changes in hyperaldosteronism?

Hypokalemia, metabolic alkalosis (due to H+ loss), hypervolemia, hypertension.

How does hypokalemia affect excitable cells?

Hyperpolarizes them, slows action potential transmission → weakness, lethargy, hyporeflexia.

What is the medical term for dilated pupils?

Mydriasis.

What is cervical ventroflexion and when is it seen?

Weakness of neck muscles causing downward head flexion, often in cats with hypokalemia (e.g., hyperaldosteronism).

How does aldosterone-driven electrolyte change affect excitable tissues?

Shifts in K+ and H+ alter membrane excitability → muscle weakness, hyporeflexia, and possible shivering.

What drug is the mineralocorticoid receptor antagonist used to treat hyperaldosteronism?

Spironolactone.

What is the therapeutic goal of spironolactone in hyperaldosteronism?

Control hypertension and hypokalemia by blocking aldosterone receptors.

Where in the nephron does spironolactone act?

Distal tubule and collecting duct mineralocorticoid receptors.

Where are mineralocorticoids produced in the adrenal gland?

Zona glomerulosa of adrenal cortex.

How are mineralocorticoids released and transported in blood?

Released on demand, mainly bound to proteins in plasma.

Summarize the main actions of aldosterone.

Promotes Na+ and water reabsorption; promotes K+ and H+ excretion; regulates BP, volume, and pH; affects excitable cell function.