Renal ammonia excretion and production in goldfish, Carassius auratus, at low environmental pH

Renal ammonia excretion and production were investigated in normal and acidotic goldfish (Carassius auratus). Goldfish were made acidotic by exposure to a low pH environment (pH 4.0), which caused a lowering of blood pH from 7.88 to 7.61. Environmental acidification resulted in an increase in total renal ammonia excretion (from 0.43 to 1.00 mueq X 100 g-1 X h-1) and urinary concentration (from 0.58 to 0.76 mM), as well as a rise in renal titratable acid output (from -0.57 to +0.62 mueq X 100 g-1 X h-1). The acidotic fish showed a rise in urine flow that was due to an increased glomerular filtration rate. In vitro studies demonstrated the capacity for renal ammonia formation from aspartate, alanine, glutamine, glutamate, and glycine. The relatively high level of glutamate in the renal tissue suggested that the generation of ammonia from these amino acids occurs via the formation of glutamate, either by deamidation of glutamine or transdeamination of aspartate and alanine. Both ammonia production by isolated renal tubules and individual enzyme assays in kidney homogenates indicated that aspartate has the greatest potential as a renal ammonia precursor in vitro. The purine nucleotide cycle, investigated with the use of the inhibitor coformycin, does not appear to contribute to ammonia production in the kidney of this species.