Effects of acid challenge on in vivo and in vitro rat renal ammoniagenesis

Abstract

This study compares the ability of different strengths of NH 4Cl, CaCl 2, and HCl to affect the termporal excretion of ammonium in rats. Oral NH 4Cl given in a single dose of 0.5 mmole, 1.0 mmole and 1.5 mmole/100 g BW steadily increases ammonium excretion in rats. The majority of the augmented ammonium excretion is secondary to increased renal production — not to changes in urine pH or urine volume. Acute challenges greater than 1.5 mmole/100 g BW do not increase ammonium excretion further. Results were similar when chronic acid challenge was investigated — greater NH 4Cl challenges cause greater ammonium excretion. Challenges beyond 1.5 mmole/100 g BW bid frequently cause death unless the rats are preconditioned (made mildly acidotic) prior to initiation of this dose. At the 1.5 mmole/100 g BW dose, maximal ammonium excretion is reached by day 2 or 3. Thus, maximal renal ammoniagenesis during acid stress occurs rapidly, and at different times depending on the strength of the acid challenge. CaCl 2 or HCl offer no advantages over NH 4Cl as acidifying agents. In addition to the above, there is a significant correlation between ammonium excretion in vivo and the ability of rat renal slices to produce ammonia from glutamine or glutamate in vitro .