A patient with primary hyperaldosteronism (Conn's syndrome) develops hypokalaemia and metabolic alkalosis. The mechanism of alkalosis is:

• A Aldosterone drives H+ secretion via H+-ATPase in alpha-intercalated cells of the collecting duct, increasing HCO3 reabsorption and new HCO3 generation; hypokalaemia further promotes H+ secretion from intracellular buffering ✓
• B Aldosterone directly stimulates proximal tubular Na+-H+ exchanger (NHE3), increasing bicarbonate reabsorption exclusively
• C Hypokalaemia alone shifts K+ out of cells in exchange for H+ ions entering cells, reducing extracellular H+ and causing alkalosis without any direct aldosterone acid-secretory effect
• D Sodium retention by aldosterone raises plasma volume, diluting H+ ions and causing contraction alkalosis

Explanation

Aldosterone has two synergistic acid-base effects in primary hyperaldosteronism. First, it upregulates H+-ATPase (vacuolar proton pump) in alpha-intercalated cells of the cortical collecting duct, directly increasing hydrogen ion secretion into the urine and generating new bicarbonate (raising plasma HCO3). Second, aldosterone increases principal cell Na+ reabsorption, creating a lumen-negative potential that drives additional K+ and H+ secretion. Third, coexisting hypokalaemia causes intracellular acidosis (K+ leaves cells in exchange for H+, drawing H+ into cells from extracellular fluid) and stimulates ammonia production, further enhancing urinary H+ excretion. Together these mechanisms produce and maintain the metabolic alkalosis. Option C is partially correct but incomplete; options B and D are not the primary mechanisms.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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