The countercurrent multiplication system in the renal medulla generates a hyperosmotic medullary interstitium. The key active transport process that powers countercurrent multiplication in the ascending thick limb of Henle's loop is:

• A Na+/H+ antiporter powered by the sodium gradient
• B NKCC2 (Na-K-2Cl cotransporter, SLC12A1) driven by the sodium gradient established by basolateral Na-K-ATPase, actively transporting NaCl into the interstitium without water (since this segment is impermeable to water) ✓
• C Urea recycling from collecting duct back into the thin limb of Henle, adding osmoles to the interstitium
• D Aquaporin-1 in the thin descending limb removing water to concentrate tubular fluid by osmosis

Explanation

The ascending thick limb of Henle (TALH) is the 'diluting segment' — it actively transports NaCl out of the tubular lumen into the interstitium via the apical NKCC2 cotransporter (target of loop diuretics like furosemide), but is impermeable to water (lacks aquaporins). This creates the 'single effect' of countercurrent multiplication: concentrated tubular fluid in the descending limb (which loses water freely via AQP1) and dilute fluid in the ascending limb, with hyperosmotic interstitium building from cortex to inner medulla. Urea recycling from the collecting duct contributes ~50% of inner medullary osmolality but is not the primary active transport process; it is a passive recycling mechanism.

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

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Written and medically reviewed by the StethoPrep medical team.