AJP - Renal Physiology, Vol 258, Issue 2 328-F332, Copyright © 1990 by American Physiological Society
Influence of acute hyponatremia on renal ammoniagenesis in dogs with chronic metabolic acidosis
M. L. Halperin and B. C. Ching
Department of Medicine, St. Michael's Hospital, University of Toronto, Ontario, Canada.
The purpose of this study was to determine how acute hyponatremia might
augment the excretion of ammonium in dogs with chronic metabolic acidosis.
The excretion of ammonium was higher during hyponatremia because the
proportion of ammonium produced that was excreted in the urine increased
from 66% in controls to 77%. Effects on the production of ammonium are more
complex. The rate of renal ammoniagenesis was not increased during
hyponatremia in absolute terms nor when expressed per millimole of oxygen
consumption. In contrast, this rate was somewhat higher during hyponatremia
if expressed per millimole of sodium reabsorbed (9.8 vs. 10.3 mumol). The
rate of oxygen consumption by the kidney did not fall, as anticipated,
during hyponatremia; when this rate was expressed per millimole of sodium
reabsorbed it rose from 46 to 55 mumol. There was no significant change in
the rate of extraction of glutamine by the kidney, but there was a
significant decrease in the rate of release of alanine during hyponatremia.
Hence there appears to be more oxidation (yielding more ammonium) and less
transamination of glutamine. We conclude that the renal events which led to
a higher rate of excretion of ammonium during hyponatremia were a larger
than expected rate of ammonium production owing to a greater rate of oxygen
consumption together with lesser rate of transamination of the glutamine
extracted by the kidney. In addition, more of the ammonium produced was
transferred to the urine.
