Renal Ammonia Production from the Nitrogens of Glutamine in Intact Acidotic Dogs before and after Bicarbonate Infusions

Abstract

Renal ammonia is produced from the amide nitrogen of glutamine, approximately 33 -50%. The remainder derives from the amino nitrogen of glutamine and other non amide sources, probably the amino nitrogens of other amino acids. We investigated the acute effects of aqid-base perturbations on ammonia production from amide and non amide nitrogen sources to determine how they interrelate. Infusions of glutamine were given to some intact dogs to vary the renal load. Following an acute alkali challenge to dogs in metabolic acidosis, ammoniagenesis from the amide nitrogens decreased significantly when the presentation of glutamine to the kidney was normal or relatively low, but changed less or even increased when the glutamine load was relatively high. In contrast, ammonia from the non amide sources consistently decreased during acute alkalotic challenge at any glutamine load -high or low. Since decreased glutamine deamination leading to glutamate accumulation is generally associated with decreased deamidation in dogs with normal plasma glutamine concentrations, we explain the discrepancy of deamidation at high glutamine loads to an unmasking of a separate effect on the glutaminase (phosphate-dependent) pathway by the acute acid-base changes. Accordingly, OUT results indicate more than one influence from acute acid-base changes in vivo on renal ammonia formation, one stimulatory and other inhibitory. Nevertheless, the influence of glutamate removal predoiniiiates over the other effect on the phosphate-dependent glutaminase pathway at physiological concentrations of glutamine in the intact dog.

Kinetics and renal effects of formic acid in occupationally exposed farmers

“…The chloride/formate exchanger is operative in the proximal tubules (Karniski and Aronson 1987), and the proximal tubular cells also liberate ammonia from glutamine and the glutamate pool (Preuss et al 1987). The exchanger could therefore maintain a higher formate concentration in these cells to cause the necessary depletion of NAD+ so that the liberation of ammonia from the glutamate would be inhibited (Preuss et al 1987).…”

“…The exchanger could therefore maintain a higher formate concentration in these cells to cause the necessary depletion of NAD+ so that the liberation of ammonia from the glutamate would be inhibited (Preuss et al 1987). This could explain the observation that urinary ammonia increases when the formate in the secondary urine in the bladder increases to discharge the acid load.…”