Stimulation of ammoniagenesis by acute acidosis: evidence for a urinary inhibitor.
To elucidate the factors mediating the response of renal ammoniagenesis to acute acidosis, the isolated perfused rat kidney was subjected to acute metabolic and respiratory acidosis with either standard collection or drainage of urine back into the perfusate. Midway during a 90-min perfusion with 0.4 mM glutamine and 5 mM glucose, perfusate pH was decreased to 6.8 by addition of HCl or alteration of the PCO2. Metabolic acidosis increased NH3 production, acidified the urine, and increased urinary NH4 excretion. Respiratory acidosis increased NH3 production to a comparable degree without urine acidification and with a minimal increase in NH4 excretion. When respiratory acidosis preceded perfusion at control PCO2 levels, NH3 production was increased but NH4 excretion was lower than control values. If urine drained back into the perfusate, NH3 production was not altered by either metabolic or respiratory acidosis. Accordingly, acute changes in perfusate pH stimulate renal ammoniagenesis by the isolated perfusate pH stimulate renal ammoniagenesis by the isolated perfused kidney independent of changes in urinary pH and NH4 excretion. This response is inhibited by an unidentified factor excreted in the urine.
D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000378:metabolism*; D000142:Acidosis, Respiratory / Q000378:metabolism*; D000641:Ammonia / Q000378:metabolism*; D000818:Animals; D004231:Diuresis; D005919:Glomerular Filtration Rate; D007668:Kidney / Q000378:metabolism*; D008297:Male; D051381:Rats
D000641:Ammonia