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.