Tannen R L
J Clin Invest. 1970 Apr;49(4):813-27. doi: 10.1172/JCI106295.
Studies were performed on normal human subjects to determine the effects of potassium depletion on urine acidification. Depletion was induced by ingestion of a low potassium diet either alone or in combination with a potassium-binding resin, and the response of each subject to an acute ammonium chloride load in the potassium-depleted state was compared to his normal response. Urine pH was significantly higher during potassium deficiency if sufficient potassium depletion had been induced. No differences in blood acid-base parameters, urinary flow rate, or urinary fixed buffer excretion rate were found to account for this change; however, the increase in urine pH was accompanied by a concomitant increase in net acid and ammonium excretion. It is proposed that these changes during potassium depletion reflect an increase in ammonia diffusion into the urine, presumably as a result of increased renal ammonia production. In addition, it is speculated that changes in ammonia metabolism may be a physiologic control mechanism for potassium conservation.
对正常人类受试者进行了研究,以确定钾缺乏对尿液酸化的影响。通过单独摄入低钾饮食或与钾结合树脂联合使用来诱导钾缺乏,并将每个受试者在钾缺乏状态下对急性氯化铵负荷的反应与其正常反应进行比较。如果诱导出足够的钾缺乏,缺钾期间尿液pH值会显著升高。未发现血液酸碱参数、尿流率或尿固定缓冲排泄率的差异可解释这种变化;然而,尿液pH值的升高伴随着净酸和铵排泄的相应增加。有人提出,钾缺乏期间的这些变化反映了氨向尿液中扩散的增加,推测这是由于肾脏氨生成增加所致。此外,据推测,氨代谢的变化可能是一种保钾的生理控制机制。