Zipp T, Tannen R L
J Lab Clin Med. 1983 Aug;102(2):198-204.
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.
通过在磷酸烯醇式丙酮酸羧激酶（PEPCK）抑制剂MPA（0.15 mM）存在的情况下灌注离体大鼠肾脏，研究了PEPCK在急性酸中毒刺激氨生成中的作用。评估了用生理量谷氨酰胺灌注的肾脏对急性呼吸性酸中毒（pCO2升高）和代谢性酸中毒（碳酸氢盐浓度降低）的反应。尽管MPA在pH 7.4时降低了肾脏氨的生成，但它对急性呼吸性或急性代谢性酸中毒所产生的氨生成刺激没有影响。因此，pH值急性下降对氨生成的刺激必定是由于对草酰乙酸转化为磷酸烯醇式丙酮酸之前的代谢步骤产生了影响。
