Wilcox C S, Granges F, Kirk G, Gordon D, Giebisch G
Am J Physiol. 1984 Sep;247(3 Pt 2):F506-19. doi: 10.1152/ajprenal.1984.247.3.F506.
Short-term hyperchloremic metabolic acidosis can decrease sodium reabsorption by the superficial proximal tubule (PT), increase tubular fluid flow rate, and stimulate aldosterone release. We studied the effects of increased tubular fluid delivery (graded saline infusion) and mineralocorticosteroid administration on tubular fluid pH (TFpH), titratable acid (TA) generation, and ammonium (NH+4) secretion by superficial proximal and distal tubules (DT) of acidotic, phosphate-loaded rats. The TFpH was 6.4 +/- 0.1 at the late proximal tubule (LP); it was unaltered at the early (ED) or late distal tubule (LD), but urine pH (UpH) was 1 unit lower. The major fraction of TA or NH+4 was formed in the superficial PT. There was no net TA generation by the superficial DT even during supplemental mineralocorticosteroid and increased Pi delivery during saline infusion. TA excretion was increased only slightly by saline infusion in acidotic rats despite increased buffer delivery (caused by decreased Pi reabsorption, primarily in the loop segment) because this was offset by a rise in UpH. Ammonia was secreted into tubular fluid in the superficial PT and DT; there was loss of NH+4 in the loop segment and addition after the LD. Saline infusion did not modify TFpH in the PT or DT but increased NH+4 secretion by the DT in direct proportion to tubular fluid flow. DOCA administration increased the addition of NH+4 between the LD and the urine. In conclusion 1) the superficial PT is of major importance for acidification, generation of TA, and secretion of NH+4 in short-term metabolic acidosis. 2) The superficial DT does not generate TA even during dramatically high rates of buffer delivery and mineralocorticosteroid administration. 3) Excretion of NH+4 is increased by saline infusion, which leads to flow-dependent NH+4 secretion by the superficial DT. 4) Chronic administration of DOCA stimulates NH+4 secretion predominantly in the terminal or deep nephrons.
短期高氯性代谢性酸中毒可减少浅表近端小管（PT）对钠的重吸收，增加肾小管液流速，并刺激醛固酮释放。我们研究了增加肾小管液输送量（分级输注生理盐水）和给予盐皮质激素对酸中毒、磷酸盐负荷大鼠浅表近端和远端小管（DT）的肾小管液pH值（TFpH）、可滴定酸（TA）生成及铵（NH₄⁺）分泌的影响。近端小管晚期（LP）的TFpH为6.4±0.1；近端小管早期（ED）或远端小管晚期（LD）的TFpH未改变，但尿pH值（UpH）降低了1个单位。TA或NH₄⁺的主要部分在浅表PT形成。即使在补充盐皮质激素以及生理盐水输注期间磷酸盐输送增加时，浅表DT也不会产生净TA。尽管酸中毒大鼠生理盐水输注时缓冲物质输送增加（主要是由于髓袢段磷酸盐重吸收减少所致），但TA排泄仅略有增加，因为这被UpH升高所抵消。氨在浅表PT和DT分泌到肾小管液中；在髓袢段有NH₄⁺丢失，在LD之后有NH₄⁺补充。生理盐水输注未改变PT或DT的TFpH，但按肾小管液流速的直接比例增加了DT的NH₄⁺分泌。给予去氧皮质酮（DOCA）增加了LD与尿液之间NH₄⁺的补充。总之，1）在短期代谢性酸中毒中，浅表PT对酸化、TA生成及NH₄⁺分泌至关重要。2）即使在缓冲物质输送速率极高和给予盐皮质激素时，浅表DT也不会产生TA。3）生理盐水输注增加了NH₄⁺排泄，导致浅表DT的NH₄⁺分泌呈流速依赖性。4）长期给予DOCA主要刺激终末或深部肾单位的NH₄⁺分泌。
