THE EFFECT OF INDUCED HYPERAMMONEMIA ON RENAL AMMONIA METABOLISM*†

Abstract

The release of ammonia into the renal veins was determined in 9 normal subjects before, during and after the intravenous administration of isotonic ammonium lactate. Concomitant measurements of urine ammonia excretion were obtained in 4 catheterized subjects and in 4 additional individuals infused with similar quantities of ammonium lactate. Hyperammonemia was associated with a prompt decrease in the amount of ammonia normally released into the renal veins with uptake of ammonia from the blood by the kidneys being observed in 8 of 9 subjects. Release reappeared and approximated control values 15 minutes after the infusion was terminated, a time when the blood ammonia concentrations were normal to slightly elevated. Urine ammonia excretion increased 2-to 3-fold during the infusion in association with a slight increase in urine pH suggesting augmented tubular secretion. The resultant of these 2 processes, however, indicates an over-all decrease in bidirectional release and presumably in total ammonia production. These observations provide additional evidence of the kidney''s role in the regulation of the blood ammonia concentration and, in addition, demonstrate that the arterial ammonia concentration significantly influences urine ammonia excretion.