Simon E, Martin D, Buerkert J
Am J Physiol. 1983 Dec;245(6):F680-6. doi: 10.1152/ajprenal.1983.245.6.F680.
The present studies were designed to assess the handling of ammonium (NH+4) by the proximal tubule during acute metabolic acidosis (AMA). After tubule fluid collections were obtained with micropuncture techniques and in situ pH was determined near the end of the proximal tubule, 0.2 N HCl was infused intravenously at 17 microliter X min-1 X 100 g body wt-1. Thirty to sixty minutes later, samples were obtained and pH measurements were made near the previous micropuncture sites. During AMA, urine pH fell and total acid excretion doubled due to an increase in NH+4 excretion from 581 +/- 63 to 1,153 +/- 61 nmol X min-1 X g kidney wt-1 (P less than 0.001). Acid excretion did not change in time controls. Tubule fluid NH+4 rose from 2.17 +/- 0.15 to 3.45 +/- 0.24 mM during acid infusion (P less than 0.001) and its delivery to the end of the proximal tubule nearly doubled (67.8 +/- 6.3 vs. 33.9 +/- 2.9 pmol X min X g kidney wt-1 before acid infusion, P less than 0.001). This increase in delivery during AMA was due to enhanced ammonia (NH3) entry into the proximal tubule. In situ pH determined near the end of the proximal tubule averaged 6.94 +/- 0.04 before acid infusion and did not change afterwards (6.87 +/- 0.05). These data are consistent with the hypothesis that in AMA the increase in NH+4 excretion is due primarily to an increase in the cortical production of NH3.
本研究旨在评估急性代谢性酸中毒（AMA）期间近端小管对铵（NH₄⁺）的处理情况。在用微穿刺技术获取小管液样本并在近端小管末端附近测定原位pH后，以17微升×分钟⁻¹×100克体重⁻¹的速率静脉输注0.2N盐酸。30至60分钟后，获取样本并在先前的微穿刺部位附近进行pH测量。在AMA期间，尿pH下降，总酸排泄量增加一倍，这是由于NH₄⁺排泄量从581±63增加到1153±61纳摩尔×分钟⁻¹×克肾重⁻¹（P＜0.001）。在时间对照组中酸排泄量没有变化。在酸输注期间，小管液NH₄⁺从2.17±0.15毫摩尔升至3.45±0.24毫摩尔（P＜0.001），其输送到近端小管末端的量几乎增加一倍（酸输注前为33.9±2.9皮摩尔×分钟×克肾重⁻¹，酸输注后为67.8±6.3皮摩尔×分钟×克肾重⁻¹，P＜0.001）。AMA期间这种输送量的增加是由于氨（NH₃）进入近端小管增强所致。在近端小管末端附近测定的原位pH在酸输注前平均为6.94±0.04，之后没有变化（6.87±0.05）。这些数据与以下假设一致：在AMA中，NH₄⁺排泄量的增加主要是由于皮质NH₃生成增加。
