Tannen R L
Med Clin North Am. 1983 Jul;67(4):781-98. doi: 10.1016/s0025-7125(16)31177-4.
The metabolic pathways involved in renal ammonia production have been considered and potential sites of regulatory control have been delineated. New information that acute acidosis stimulates renal ammonia production and that chronic respiratory acidosis does not result in an adaptive increase in the renal capacity to produce ammonia has been emphasized. The effect of potassium on renal ammonia production and the physiologic and pathophysiologic implication of this relationship have been detailed. Finally, the mechanism of urinary ammonium excretion and the impact of altered ammoniagenesis on urinary acidification, and the interpretation of clinical acidification tests have been discussed.
已经对参与肾脏氨生成的代谢途径进行了探讨,并确定了潜在的调控部位。着重强调了新的信息,即急性酸中毒会刺激肾脏氨生成,而慢性呼吸性酸中毒不会导致肾脏氨生成能力的适应性增加。详细阐述了钾对肾脏氨生成的影响以及这种关系的生理和病理生理意义。最后,讨论了尿铵排泄的机制、氨生成改变对尿液酸化的影响以及临床酸化试验的解读。