Amiloride, triamterene, and the spirolactones are potassium-sparing diuretics which act on the distal parts of the nephron, from the late distal tubule to the collecting duct. In these segments, active sodium reabsorption occurs through the following mechanism: sodium ions enter the cell through specific channels present in the luminal membrane and are extruded out of the cell into the peritubular medium by a sodium-potassium exchange pump, the Na-K-ATPase. Amiloride in micromolar concentrations reduces the sodium transport by blocking the luminal membrane sodium channel. Triamterene has a similar effect, although with a lower affinity; the available studies do not allow to determine if an inhibitory effect of triamterene on the Na-K-ATPase plays an additional role in its diuretic action. The spirolactones are competitive inhibitors of aldosterone, the mineralocorticoid hormone which promotes sodium reabsorption by increasing both the number of active sodium channels in the luminal membrane and the number of active Na-K pumps in the peritubular membrane. By the inhibitory effect on the electrogenic sodium transport, amiloride, triamterene, and the spirolactones decrease the lumen-negative transepithelial potential difference. This reduces the driving force for potassium movement into the tubular lumen and thus decreases potassium excretion.