Regarding renal compensation in respiratory acidosis, which tubular mechanism is MOST important for the delayed (2–5 day) rise in plasma HCO3⁻?

• A Increased PCT H⁺-ATPase activity causing more HCO3⁻ reclamation from filtered load
• B Decreased chloride reabsorption in the thick ascending limb increasing HCO3⁻ relative concentration
• C Enhanced collecting duct alpha-intercalated cell H⁺ secretion coupled with new HCO3⁻ generation via glutamine metabolism and titratable acid excretion ✓
• D Carbonic anhydrase-independent bicarbonate generation in the distal tubule

Explanation

Renal compensation for chronic respiratory acidosis involves generation of NEW bicarbonate, not mere reclamation of filtered HCO3⁻ (which is already nearly complete in proximal tubule). Alpha-intercalated cells of the collecting duct secrete H⁺ via H⁺-ATPase and H⁺/K⁺-ATPase, generating new HCO3⁻ that enters the blood. Additionally, enhanced ammoniagenesis (glutamine catabolism in PCT) allows excretion of NH4⁺ carrying acid, producing new HCO3⁻. This process takes 2–5 days to fully compensate. Carbonic anhydrase II and IV are essential; the process is not CA-independent.

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

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