Expansion
Sodium in, potassium and hydrogen out, at the distal nephron
Expansion
Acting on principal cells of the late distal tubule and collecting duct:
- Increases epithelial sodium channels (ENaC) on the apical membrane
- Increases the sodium-potassium ATPase on the basolateral membrane
- Result: sodium reabsorption, with water following, and potassium secretion
- Also stimulates hydrogen ion secretion by intercalated cells
Stimuli: angiotensin II, hyperkalaemia (a direct and powerful stimulus), and ACTH to a minor degree.
Excess (Conn syndrome, secondary hyperaldosteronism): hypertension, hypokalaemia and a metabolic alkalosis. Note that oedema does not usually occur, because of aldosterone escape: rising volume increases atrial natriuretic peptide and pressure natriuresis.
Deficiency (Addison disease): hyponatraemia, hyperkalaemia, metabolic acidosis and hypovolaemia.
Drugs: spironolactone and eplerenone block the receptor, while amiloride blocks ENaC directly; both are potassium sparing.