Pressure natriuresis
Pressure natriuresis is the extra sodium excreted in the urine when renal artery pressure rises, because the proximal tubule (the first coiled section of the nephron) reabsorbs less.
Remember
When pressure in the renal artery rises, the proximal tubule reabsorbs less sodium, so more sodium and water are excreted and blood pressure falls.
When pressure in the renal artery (the artery that supplies the kidney) rises, the cells of the proximal convoluted tubule reabsorb less sodium. Normally this segment reabsorbs about 65% of the filtered sodium and water.
Fewer sodium-hydrogen exchangers (membrane proteins that swap sodium into the cell for hydrogen out of it) remain at the surface facing the lumen. The sodium-potassium ATPase (the pump on the blood side of the cell that powers sodium reabsorption) is also less active. With less sodium taken back, less water follows it by osmosis, so more sodium and water leave in the urine.
The extra sodium excretion is called pressure natriuresis, and the extra water excretion is pressure diuresis. Intravascular volume (the fluid within the blood vessels) then falls, and blood pressure falls with it. That makes the process a negative feedback loop, because it opposes a rise in blood pressure. It is the kidney's own response to pressure and needs no hormone.
Key facts
- Trigger
- A rise in the pressure in the renal artery.
- Site
- The proximal convoluted tubule, which normally reabsorbs about two-thirds of the filtered sodium.
- Mechanism
- Fewer sodium-hydrogen exchangers and lower sodium-potassium ATPase activity.
- Result
- More sodium and water are excreted, so intravascular volume and blood pressure fall.
- Names
- Pressure natriuresis is the extra sodium excretion, and pressure diuresis is the extra water excretion.
- Control
- The response of the kidney to pressure itself needs no hormone.
Exam traps
- Sodium-glucose cotransporters (which reabsorb sodium and glucose in the proximal tubule) would lower sodium reabsorption if they were less active, but they are not the transport change that a rise in renal artery pressure triggers.
- Aldosterone, which regulates sodium reabsorption, does not produce pressure natriuresis: increased aldosterone release enhances reabsorption, retaining sodium and water.
- The sodium-potassium ATPase is the right pump in the right segment, but the direction is wrong: it drives proximal sodium reabsorption, so a rise in perfusion pressure reduces its activity rather than increasing it.
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