Complementary role of citrate and bicarbonate excretion in acid-base balance in the rat.

Studies were performed to evaluate whether alterations in the excretion of citrate, a metabolic precursor of bicarbonate, play a quantitatively important role in acid-base balance during bicarbonate feeding in the rat. Potassium depletion (K-DEPL), chloride depletion (Cl-DEPL), or potassium plus chloride depletion (KCl-DEPL) was produced by eliminating potassium, chloride, or potassium chloride from the diet. After 3 days of depletion, sodium bicarbonate (4,000 mueq/24 h) was added to the diet for 7 days. In all groups plasma bicarbonate concentration increased minimally during bicarbonate administration and was similar to normal controls receiving bicarbonate. In K-DEPL, citrate excretion was less than normal but bicarbonate excretion was greater than normal. In Cl-DEPL, bicarbonate excretion was less than normal but citrate excretion was greater than normal. In KCl-DEPL, bicarbonate and citrate excretion were similar to normal. Sodium bicarbonate was also administered to K-DEPL and KCl-DEPL rats in which plasma bicarbonate concentration averaged 32.9 meq/1. The reciprocal relationship between citrate and bicarbonate excretion was not altered by the profound metabolic alkalosis. Again, plasma bicarbonate concentration changed little with sodium bicarbonate administration. These studies suggest that the ability to excrete a base load remains intact despite potassium or chloride depletion or metabolic alkalosis. Complementary alterations of citrate and bicarbonate excretion play an important role in acid-base balance under these conditions.