An experimental preparation doubles single-nephron glomerular filtration rate, doubling distal tubular flow rate and sodium delivery, while circulating aldosterone is clamped constant. What happens to potassium secretion by the cortical collecting duct?
- A It rises substantially, because faster flow washes secreted potassium away and sustains the concentration gradient favoring ROMK-mediated secretion ✓
- B It falls, because higher flow dilutes aldosterone in tubular fluid
- C It is unchanged, since aldosterone alone determines potassium secretion
- D It reverses direction, with the duct reabsorbing potassium through H-K ATPase
Explanation
Potassium secretion by principal cells depends not only on aldosterone but also on tubular flow rate and distal sodium delivery. Rapid flow sweeps secreted potassium downstream, keeping luminal potassium low and preserving the favorable electrochemical gradient across the apical ROMK channel, while delivered sodium enters through ENaC and depolarizes the cell to drive secretion. This is why loop diuretics cause kaliuresis even before aldosterone changes, and why oliguric states predispose to hyperkalemia despite normal mineralocorticoid levels. H-K ATPase mediates potassium reabsorption mainly under potassium depletion.
Reference: Vander's Renal Physiology, 8th ed.
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