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Which renal tubular change most directly explains the phenomenon of pressure natriuresis when renal arterial blood pressure rises?

Reduced epithelial sodium channel activity in the proximal convoluted tubule leading to less sodium reabsorption Reduced sodium-potassium ATPase activity in the collecting duct intercalated cells leading to less sodium reabsorption Reduced sodium-hydrogen exchanger activity in the proximal convoluted tubule leading to less sodium reabsorption Reduced sodium-glucose cotransporter activity in the proximal convoluted tubule leading to less sodium reabsorption Reduced sodium-hydrogen exchanger activity in the collecting duct principal cells leading to less sodium reabsorption

A Reduced epithelial sodium channel activity in the proximal convoluted tubule leading to less sodium reabsorption
B Reduced sodium-potassium ATPase activity in the collecting duct intercalated cells leading to less sodium reabsorption
C Reduced sodium-hydrogen exchanger activity in the proximal convoluted tubule leading to less sodium reabsorption ✓
D Reduced sodium-glucose cotransporter activity in the proximal convoluted tubule leading to less sodium reabsorption
E Reduced sodium-hydrogen exchanger activity in the collecting duct principal cells leading to less sodium reabsorption

The answer is C: Reduced sodium-hydrogen exchanger activity in the proximal convoluted tubule leading to less sodium reabsorption

Explanation

Why C is correct

See Pressure Natriuresis and Diuresis. Option C is correct: when blood pressure in the renal artery rises, there are fewer sodium-hydrogen (Na-H) exchangers in the proximal convoluted tubule, so less sodium is reabsorbed. The Na-H exchanger is a membrane protein that swaps one hydrogen ion out of the cell for one sodium ion in from the tubular fluid, and it is a major route for sodium reabsorption in the proximal tubule. The activity of the sodium-potassium ATPase, the basolateral pump that keeps the cell's sodium low and drives all this uptake, also falls. With less sodium reclaimed, more sodium stays in the tubular fluid. Water follows the extra sodium by osmosis, so more water is also lost. The kidney therefore loses sodium (pressure natriuresis) and water (pressure diuresis). The intravascular volume falls and with it blood pressure, which makes this a built-in negative feedback loop that opposes a rise in blood pressure. Memory aid: pressure up, pumps down, sodium out.

Proximal tubule: higher renal arterial pressure means fewer sodium-hydrogen exchangers, so less sodium is reabsorbed.
Pump: sodium-potassium ATPase activity also falls.
Result: more sodium and water are lost, so volume and blood pressure fall in a negative feedback loop.

Why the other options are incorrect

A. Reduced epithelial sodium channel activity in the proximal convoluted tubule leading to less sodium reabsorption: Epithelial sodium channels are the sodium entry step in the late distal tubule and collecting duct, not in the proximal convoluted tubule, so this change is not the mechanism of pressure natriuresis.
B. Reduced sodium-potassium ATPase activity in the collecting duct intercalated cells leading to less sodium reabsorption: Intercalated cells are acid-base cells and are not the main sodium-reabsorbing cells of the collecting duct, so reduced sodium-potassium ATPase activity there would not explain pressure natriuresis.
D. Reduced sodium-glucose cotransporter activity in the proximal convoluted tubule leading to less sodium reabsorption: Reduced sodium-glucose cotransport in the proximal tubule would lower sodium reabsorption, but this cotransporter is not the transport change triggered by a rise in renal artery pressure.
E. Reduced sodium-hydrogen exchanger activity in the collecting duct principal cells leading to less sodium reabsorption: Principal cells of the collecting duct reabsorb sodium through epithelial sodium channels, not sodium-hydrogen exchangers, so reduced Na-H exchange in these cells is not the mechanism.

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1
Which membrane protein is primarily responsible for driving sodium reabsorption throughout the nephron by creating the necessary electrochemical gradient?
2
Which transporter in the early distal convoluted tubule is electroneutral and is the primary site of action of thiazide diuretics?

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