Lecture on Aldosterone

Overview

• Aldosterone is a hormone crucial for regulating blood pressure and blood volume.
• Increases sodium reabsorption by the kidneys.
• Secreted from the zona glomerulosa of the adrenal cortex.
• Uses cholesterol to make aldosterone and other mineralocorticoids.
• Hydrophobic nature; transported in the blood bound to albumin.

Secretion and Regulation

• Released under conditions of low blood pressure.
• Increases When:
  • Angiotensin II or potassium levels increase in blood and extracellular fluid.
• Decreases When:
  • Sodium ion concentration increases in the extracellular fluid.

Mechanism of Action

• Aldosterone diffuses into the principal epithelial cells of the late distal tubules and cortical collecting tubules.
• Binds with mineralocorticoid receptor to form aldosterone-receptor complex in cytoplasm.
• Complex enters nucleus, upregulates transcription of DNA into mRNA.
• mRNA is translated into proteins that enhance sodium reabsorption, potassium, and hydrogen secretion.
• Increases sodium-potassium pump formation on basolateral membrane of principal cells.
• Increases expression of epithelial sodium channels (ENaC) on the apical membrane.
• Action of ENaC and sodium-potassium pumps facilitate sodium movement from filtrate to renal capillaries.

Effects on Fluid and Electrolyte Balance

• Sodium attracts water, increasing serum sodium levels and fluid volume.
• Elevates blood pressure.
• Principal cells secrete potassium into the tubular lumen due to intracellular concentration gradient.
• Aldosterone boosts hydrogen-potassium pump activity on the apical membrane of type A intercalated cells, causing increased hydrogen secretion (alkalosis).

Primary Aldosteronism (Kahn Syndrome)

• Tumor in zona glomerulosa cells secretes excessive aldosterone.
• Symptoms include:
  • Hypokalemia (low potassium levels)
  • Mild metabolic alkalosis
  • Modest increase in ECF and blood volume
  • Often high blood pressure
  • Edema often not present due to atrial natriuretic hormone release.
  • Increased sodium levels in blood by 4-6 mEq/L.
  • Changes in resting potential of neurons (hyperpolarization), causing muscle weakness.
• Diagnostic feature: Decreased plasma renin levels.
• Treatment:
  • Surgical removal of tumor.
  • Management of hypertension and hypokalemia before surgery.
  • Aldosterone antagonist like spironolactone.

Secondary Aldosteronism

• Due to extra-adrenal stimuli (often increased renin production).
• Occurs with decreased circulating blood volume (shock, dehydration, liver failure).
• Liver failure leads to decreased blood colloid osmotic pressure (insufficient albumin production).
• Less blood delivery to kidneys (renal artery stenosis, heart failure) increases aldosterone.
• Renin-secreting tumors can also cause secondary aldosteronism.