Aldosterone

Aldosterone tends to promote Na+ and water retention, and lower plasma K+concentration by the following mechanisms:

  1. Acting on the nuclear mineralocorticoid receptors (MR) within the principal cells of the distal tubule and the collecting duct of the kidney nephron, it upregulates and activates the basolateral Na+/K+ pumps, which pumps three sodium ions out of the cell, into the interstitial fluid and two potassium ions into the cell from the interstitial fluid. This creates a concentration gradient which results in reabsorption of sodium (Na+) ions and water (which follows sodium) into the blood, and secreting potassium (K+) ions into the urine (lumen of collecting duct).
  2. Aldosterone upregulates epithelial sodium channels (ENaCs) in the collecting duct and the colon, increasing apical membrane permeability for Na+ and thus absorption.
  3. Cl− is reabsorbed in conjunction with sodium cations to maintain the system's electrochemical balance.
  4. Aldosterone stimulates the secretion of K+ into the tubular lumen.[9]
  5. Aldosterone stimulates Na+ and water reabsorption from the gut, salivary and sweat glands in exchange for K+.
  6. Aldosterone stimulates secretion of H+ via the H+/ATPase in the intercalated cells of the cortical collecting tubules
  7. Aldosterone upregulates expression of NCC in the distal convoluted tubule chronically and its activity acutely.[10]

Aldosterone is responsible for the reabsorption of about 2% of filtered sodium in the kidneys, which is nearly equal to the entire sodium content in human blood under normal glomerular filtration rates

Hyperaldosteronism

Excessive ingestion of black licorice can mimic hyperaldosteronism

Primary hyperaldosteronism (aka Conn's syndrome)

  1. Hypertension
  2. hypokalemia (>20% may be normokalemic)
  3. Metabolic alkalosis,
  4. Na+ may be raised or normal

Basic Science Correlate