Regulation of the maximum rate of renal ammoniagenesis in the acidotic XXXX .

@entity34085 @entity1160 @entity235 @entity1792 @entity26 @entity1372 @entity880 @entity3104 @entity493 @entity413 @entity855
Metabolism of @entity1160 results in the net production of @entity855 ; however, cells cannot sustain an @entity855 production rate greater than their rate of @entity855 utilization. The purpose of these studies was to determine whether the rate of @entity855 turnover in the kidney could set an upper limit on renal @entity1160 metabolism and thereby renal ammoniagenesis. The acidotic @entity235 kidneys extracted @entity1160 , @entity880 , @entity1792 , and @entity26 from the arterial blood and added @entity3104 and @entity493 to the venous blood. Renal @entity1160 metabolism was responsible for almost all the @entity3104 production. Renal @entity855 production was estimated from the rate of @entity26 consumption and appeared to be derived roughly equally from the oxidation of @entity1160 and @entity880 . There was no apparent renal @entity413 production from @entity855 balance calculations and this impression was supported when the inhibitor of gluconeogenesis, @entity34085 , did not inhibit ammoniagenesis. Approximately 90% of the @entity855 synthesized was utilized to reabsorb @entity1372 . When the amount of @entity855 utilized for @entity1372 reabsorption in the proximal convoluted tubule (assumed to be 60% of filtered @entity1372 ) was compared with the amount of @entity855 produced from @entity1160 metabolism, the values were similar despite the fact that the glomerular filtration rate in individual @entity235 varied more than fourfold. When the quantity of @entity855 expended for @entity1372 reabsorption was decreased by the infusion of ouabain or by the constriction of one renal artery without reducing @entity1160 delivery, the kidney lowered its rate of ammoniagenesis to a quantitatively predictable amount.(ABSTRACT TRUNCATED AT 250 WORDS)
