Abstract
Summary
SHR excrete less ammonium than NWR and SD following water load and acute and chronic acidosis. Thus, their ability to handle acute and chronic acid challenge is impaired because of the lesser ammonium excretion. Since these differences in ammonium excretion cannot be related in entirety to urine flow, urine pH, and kidney mass, basic differences in vivo in renal metabolism of glutamine, the major precursor of renal ammonia, seem likely. Slices from chronically acidotic SHR compared to slices from chronically acidotic NWR produce less ammonia, suggesting some basic intrinsic difference in renal glutamine metabolism during persistent acidosis. Because these differences in slice ammoniagenesis are smaller than the differences in ammonium excretion, and because slices from nonaci-dotic SHR and NWR show no differences in ammoniagenesis, we feel that other in vivo factors, probably extrarenal, additionally decrease renal ammonia production in SHR.
Get full access to this article
View all access options for this article.
