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.