The distal convoluted tubule is a water-impermeable segment of the nephron that continues the dilution of luminal fluid through active sodium chloride absorption.

Sodium absorption in the distal nephron occurs primarily by a thiazide diuretic-sensitive, chloride-coupled transport process. The cortical collecting duct reabsorbs sodium by a mineralocorticoid-sensitive process. In states of volume depletion and maximal aldosterone production, the urine can be rendered virtually free of sodium.

Because the cortical interstitium remains isotonic to plasma, salt absorption from these segments affects urinary dilution but not urinary concentration. Potassium secretion begins in the distal convoluted tubule and continues along the collecting ducts. Virtually all of the filtered potassium is reabsorbed in proximal nephron segments, and the potassium that appears in the urine is mostly a result of secretion by the distal nephron segments. Potassium secretion proceeds by diffusion of the intracellular cation down both concentration and electrical gradients into the tubular lumen. The principal cell in the collecting duct is the major site of potassium secretion. The basolateral Na,K-ATPase establishes the concentration gradient by maintaining a high intracellular potassium concentration. The potassium is then secreted into the tubular lumen down its concentration gradient through a potassium channel. Although some potassium may leak back across the basolateral membrane, two factors favor the movement of potassium into the luminal fluid First, the concentration of potassium in the luminal fluid is low.

enhanced distal tubular flow thus results in the mainte nance of low intraluminal potassium concentrations and stimulates potassium secretion. Second, the principal have a sodium channel on the apical side which results in sodium reabsorption from the tubular lumen.

This results in a negative electrical potential in the tubular lumen that favors the movement of potassium from the cell into the tubular lumen.