AJP - Regulatory, Integrative and Comparative Physiology, Vol 245, Issue 4 581-R589, Copyright © 1983 by American Physiological Society
Renal ammoniagenesis and acid excretion in the dogfish, Squalus acanthias
P. A. King and L. Goldstein
Renal ammoniagenesis and acid excretion were investigated in normal dogfish
(Squalus acanthias) and dogfish made acidotic by HCl injection (0.65 meq X
kg-1). After acid loading, renal ammonia excretion doubled, rising from
0.11 to 0.25 mueq X h-1, and titratable acid output increased from 28.6 to
44.9 mueq X h-1. Trimethylamine excretion averaged 23.2 mueq X h-1 and did
not change in response to the acidosis. During the first 24 h
postinjection, the increase in renal acid excretion accounted for the
elimination of 15% of the acid load. In vitro studies with kidney slices
demonstrated that the dogfish kidney has the capacity to synthesize ammonia
from a number of amino acids including glutamine, glutamate, alanine,
aspartate, and glycine, with the greatest ammonia production resulting from
glutamine. The relatively high glutamine concentration in the kidney,
compared with the blood, suggested a high renal capacity for glutamine
synthesis. In renal homogenates, enzymatic activities for both the
deamidation (glutaminase) and synthesis (glutamine synthetase) of glutamine
were investigated. The Michaelis constant (Km) values for the two enzymes
were found to be almost equal (4.48 mM glutamine and 4.33 mM glutamate) and
at the same levels as the substrate concentrations in the kidney (3.69 mM
glutamine and 3.36 mM glutamate). Subcellular localization revealed that
both enzymes occur predominantly in the mitochondria. The activities of
glutaminase and glutamine synthetase in the renal mitochondria suggest the
presence of a substrate cycle that could be modulated to increase ammonia
production during acidosis.
