Melton L B, Frazier L W, Vanatta J C
Biochim Biophys Acta. 1979 Jun 1;585(1):53-60. doi: 10.1016/0304-4165(79)90324-6.
It is well known that ammonium ion excretion is increased during metabolic acidosis in mammals. The purpose of this study was to determine whether we could isolate from human urine during metabolic acidosis a factor that would stimulate NH+4 and/or H+ excretion in toad urinary bladder. Extracts of urine from six human subjects collected during NH4Cl-induced acidosis were prepared. These extracts were tested for their effect on NH+4 excretion in hemibladders mounted between plastic chambers. The extracts significantly increased NH+4 excretion in the toad urinary bladder. We found no effect on H+ excretion by these extracts. This ammoniuretic activity was not present in the urine when the same individuals were in metabolic alkalosis. We conclude that during metabolic acidosis a humoral factor is present which stimulates the excretion of NH+4. The factor could act as a permease in the bladder cell or as a stimulator of an NH+4 transport system.
众所周知，在哺乳动物的代谢性酸中毒期间铵离子排泄会增加。本研究的目的是确定我们是否能够在代谢性酸中毒期间从人尿中分离出一种能刺激蟾蜍膀胱中NH₄⁺和/或H⁺排泄的因子。制备了在氯化铵诱导的酸中毒期间收集的六名人类受试者的尿液提取物。测试了这些提取物对安装在塑料室之间的半膀胱中NH₄⁺排泄的影响。这些提取物显著增加了蟾蜍膀胱中的NH₄⁺排泄。我们发现这些提取物对H⁺排泄没有影响。当同一个体处于代谢性碱中毒时，这种利尿铵活性在尿液中不存在。我们得出结论，在代谢性酸中毒期间存在一种体液因子，它刺激NH₄⁺的排泄。该因子可能在膀胱细胞中充当通透酶或充当NH₄⁺转运系统的刺激物。
