Influence of phosphoenolpyruvate carboxykinase inhibition on the response of NH3 production to acute acidosis.
The role of PEPCK in the stimulation of NH3 production by acute acidosis was examined by perfusing isolated rat kidneys in the presence of the PEPCK inhibitor, MPA (0.15 mM). The response of kidneys perfused with physiologic quantities of glutamine to both acute respiratory (increase in pCO2) and metabolic acidosis (decrease in bicarbonate concentration) was assessed. Although MPA decreased renal NH3 production at pH 7.4, it had no effect on the stimulation of ammoniagenesis produced by either acute respiratory or acute metabolic acidosis. Thus the stimulation of NH3 production by an acute decline in pH must result from an effect on a metabolic step prior to the conversion of oxaloacetate to phosphoenolpyruvate.
D000138:Acidosis / Q000378:metabolism* / Q000652:urine; D000641:Ammonia / Q000378:metabolism*; D000818:Animals; D005973:Glutamine / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D007668:Kidney / Q000378:metabolism*; D008297:Male; D010477:Perfusion; D010729:Phosphoenolpyruvate Carboxykinase (GTP) / Q000037:antagonists & inhibitors*; D010848:Picolinic Acids / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D010848:Picolinic Acids; D005973:Glutamine; D000641:Ammonia; C008363:3-mercaptopicolinic acid; D010729:Phosphoenolpyruvate Carboxykinase (GTP)