Potassium-depletion alkalosis in the rat.

Studies were performed to investigate the role of concomitant chloride depletion in potassium-depletion alkalosis in the rat and the relationship between potassium depletion, plasma bicarbonate (PHCO3), and net acid excretion. 1) Selective potassium depletion (K-DEPL), potassium plus chloride depletion (KCl-DEPL), or selective chloride depletion (Cl-DEPL) was produced by administering a selectively potassium-, potassium and chloride-, or selectively chloride-deficient diet. In K-DEPL and KCl-DEPL rat, PHCO3 increased progressively and similarly during a 38-day period of restriction, whereas net acid excretion was similar and not elevated in either group. Cl-DEPL did not result in alkalosis. Chloride administration without potassium in alkalotic KCl-DEPL rats did not result in a sustained significant decrease in PHCO3. Potassium administration without chloride in alkalotic KCl-DEPL rats decreased PHCO3. Thus concomitant chloride depletion plays a minimal role in the alkalosis produced by dietary-induced potassium depletion. 2) Administration of a chronic acid load to alkalotic K-DEPL rats did not decrease PHCO3, and net acid excretion increased similarly as in normals. In K-DEPL rats after PHCO3 was reduced toward normal levels with acetazolamide, net acid excretion increased sharply above base-line values and PHCO3 increased markedly. Thus the alkalotic K-DEPL rat maintains the ability to excrete a chronic acid load, and a reduction in PHCO3 elicits an increase in acid excretion to restore the initial acid-base condition. These studies suggest that potassium depletion alters the set-point at which the kidney maintains PHCO3.