Pressure-natriuresis is the direct intrinsic renal mechanism by which elevated arterial pressure increases sodium and water excretion. The key intracellular mediator that reduces proximal tubule NHE3 activity during pressure-natriuresis is:

• A Local generation of intrarenal angiotensin II that stimulates NHE3 to increase sodium reabsorption
• B Decreased prostaglandin E2 that increases medullary blood flow and washes out the corticomedullary gradient
• C Increased plasma aldosterone that stimulates ENaC in the collecting duct independently of pressure
• D Increased renal interstitial hydrostatic pressure that reduces basolateral Na-K-ATPase activity and increases the paracellular back-leak of NaCl ✓

Explanation

When arterial pressure rises, medullary blood flow through vasa recta increases, washing out the medullary osmotic gradient. More importantly, increased capillary pressure in the peritubular capillaries raises peritubular and interstitial hydrostatic pressure in the cortex. This: (1) reduces the driving force for basolateral fluid absorption (via Starling forces), and (2) increases back-flux of reabsorbed fluid through paracellular junctions. Both effects reduce net sodium reabsorption in the proximal tubule. Additionally, increased pressure may reduce local angiotensin II (which normally stimulates NHE3), further dampening Na⁺ reabsorption. This renal-pressure response is the ultimate long-term BP stabilizer.

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

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