Simon E, Martin D, Buerkert J
J Clin Invest. 1985 Aug;76(2):855-64. doi: 10.1172/JCI112043.
Ammonia entry along surface nephron segments of rats was studied with micropuncture techniques under control and chronic metabolic acidosis conditions. Tubule fluid was collected successively from sites at the end and beginning of the distal tubule and at the end of the proximal tubule of the same nephron. During chronic metabolic acidosis, ammonium excretion doubled. As anticipated, the ammonium concentration (TFNH+4) was significantly higher in proximal tubule fluid during acidosis, and ammonium delivery to end proximal sites increased from 19.4 +/- 2.3 to 34.0 +/- 3.2 pmol/min (P less than 0.001). Although chronic acidosis did not affect TFNH+4 at the beginning of the distal tubule, ammonium delivery to the end of the distal tubule increased from 5.72 +/- 0.97 to 9.88 +/- 0.97 pmol/min. In both control and acidotic groups ammonium delivery was lower (P less than 0.001) to end distal sites than to end proximal sites, indicating net loss in the intervening segment. This loss was greater during chronic metabolic acidosis (23.9 +/- 3.3 vs. 13.6 +/- 2.0 pmol/min in controls, P less than 0.025). In both groups net entry of ammonia, in similar amounts, occurred along the distal tubule (P less than 0.05). In situ pH averaged 6.80 +/- 0.05 at end proximal tubule sites and fell to 6.54 +/- 0.08 at the beginning of the distal tubule (P less than 0.005). Chronic metabolic acidosis did not affect these measurements. The calculated free ammonia at the end of the proximal tubule rose from 9.3 +/- 2.2 to 21 +/- 9 microM (P less than 0.005) during chronic metabolic acidosis, and was also higher at beginning distal sites during acidosis (8.8 +/- 2.4 vs. 2.7 +/- 0.7 microM in controls, P less than 0.05). In both groups ammonia values for the beginning distal tubule fluid were lower than for end proximal tubule fluid. Thus, loss of ammonium in the loop segment is enhanced by chronic metabolic acidosis. Distal entry of ammonia is markedly less than along the proximal tubule and does not change in chronic metabolic acidosis, and ammonia permeabilities for the proximal and distal segments of surface nephrons seem different.
采用微穿刺技术，在对照和慢性代谢性酸中毒条件下，研究了大鼠肾单位表面节段的氨进入情况。从同一条肾单位远曲小管末端和起始端以及近曲小管末端的部位依次收集小管液。在慢性代谢性酸中毒期间，铵排泄量增加了一倍。正如预期的那样，酸中毒期间近曲小管液中的铵浓度（TFNH+4）显著更高，并且输送到近曲小管末端部位的铵从19.4±2.3皮摩尔/分钟增加到34.0±3.2皮摩尔/分钟（P<0.001）。虽然慢性酸中毒不影响远曲小管起始端的TFNH+4，但输送到远曲小管末端的铵从5.72±0.97皮摩尔/分钟增加到9.88±0.97皮摩尔/分钟。在对照组和酸中毒组中，输送到远曲小管末端部位的铵均低于输送到近曲小管末端部位的铵（P<0.001），表明中间节段有净损失。在慢性代谢性酸中毒期间这种损失更大（对照组为13.6±2.0皮摩尔/分钟，酸中毒组为23.9±3.3皮摩尔/分钟，P<0.025）。在两组中，沿远曲小管都有相似量的氨净进入（P<0.05）。近曲小管末端部位的原位pH平均为6.80±0.05，在远曲小管起始端降至6.54±0.08（P<0.005）。慢性代谢性酸中毒不影响这些测量值。在慢性代谢性酸中毒期间，近曲小管末端计算出的游离氨从9.3±2.2微摩尔升至21±9微摩尔（P<0.005），并且在酸中毒期间远曲小管起始端的游离氨也更高（对照组为2.7±0.7微摩尔，酸中毒组为8.8±2.4微摩尔，P<0.05）。在两组中远曲小管起始端小管液的氨值均低于近曲小管末端小管液的氨值。因此，慢性代谢性酸中毒会增强袢段中铵的损失。远曲小管的氨进入明显少于近曲小管，并且在慢性代谢性酸中毒中不变，表面肾单位近曲和远曲节段的氨通透性似乎不同。
