Terao N, Tannen R L
Am J Physiol. 1980 Nov;239(5):F445-51. doi: 10.1152/ajprenal.1980.239.5.F445.
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.
为阐明介导肾产氨对急性酸中毒反应的因素，对离体灌注大鼠肾脏进行急性代谢性和呼吸性酸中毒处理，同时将尿液标准收集或回输至灌注液中。在用0.4 mM谷氨酰胺和5 mM葡萄糖进行90分钟灌注的过程中，通过添加盐酸或改变PCO2将灌注液pH降至6.8。代谢性酸中毒增加了NH3生成，使尿液酸化，并增加了尿NH4排泄。呼吸性酸中毒使NH3生成增加至相当程度，但未使尿液酸化，且NH4排泄仅有最小程度增加。当在对照PCO2水平下呼吸性酸中毒先于灌注发生时，NH3生成增加，但NH4排泄低于对照值。如果尿液回输至灌注液中，代谢性或呼吸性酸中毒均不会改变NH3生成。因此，灌注液pH的急性变化可通过离体灌注肾脏刺激肾产氨，这一刺激独立于尿液pH和NH4排泄的变化。该反应受到尿液中一种未知因素的抑制。
