Kornandakieti C, Tannen R L
Kidney Int. 1984 Apr;25(4):629-35. doi: 10.1038/ki.1984.67.
The effect of aldosterone on distal nephron acidification was investigated by comparing isolated perfused kidneys from adrenalectomized rats treated for 3 to 5 days with dexamethasone alone (10 micrograms/day i.p.) and from rats given in addition a physiologic dose of d-aldosterone (10 micrograms/day in oil s.c.). The maximal pH gradient between urine and perfusate, determined at a perfusate pH of 6.7 with glucose as the sole substrate, did not differ significantly between the aldosterone deplete and replete groups (1.27 +/- 0.12 vs. 1.35 +/- 0.12). H+ secretory capacity of the distal nephron was determined by perfusing kidneys at pH 6.8 and providing saturating quantities of urinary buffer in the form of creatinine. Under these experimental conditions kidneys from aldosterone deplete rats had a higher urine pH and lower excretion rate of titratable acid indicative of a defect in H+ secretion. Acid secretion below a pH of 6.0 (T.A.-pH 6.0), an index of H+ secretion by the distal nephron, was also significantly lower in the aldosterone deplete kidneys. Thus, aldosterone depletion decreased the H+ secretory capacity of the distal nephron, but had no clear effect on the force of the pump as reflected by the maximal pH gradient. Amiloride (10(-5) M) was added to the perfusate of kidneys undergoing the H+ secretory capacity protocol to distinguish between sodium-linked and sodium-independent effects of aldosterone. The difference in T.A. pH 6.0 between aldosterone deplete and replete kidneys was reduced by approximately 70% in the presence of amiloride. This indicates that a substantial portion of the aldosterone-dependent component of distal nephron H+ secretion is mediated by a sodium-dependent mechanism.
通过比较以下两组大鼠的离体灌注肾脏，研究了醛固酮对远端肾单位酸化的影响：一组是接受地塞米松（10微克/天，腹腔注射）单独治疗3至5天的肾上腺切除大鼠，另一组是除地塞米松外还给予生理剂量的d -醛固酮（10微克/天，皮下注射于油中）的大鼠。以葡萄糖作为唯一底物，在灌注液pH为6.7时测定的尿液与灌注液之间的最大pH梯度，在醛固酮缺乏组和补充组之间无显著差异（分别为1.27±0.12和1.35±0.12）。通过在pH 6.8下灌注肾脏并以肌酐形式提供饱和量的尿液缓冲剂来测定远端肾单位的H⁺分泌能力。在这些实验条件下，醛固酮缺乏大鼠的肾脏尿液pH较高，可滴定酸排泄率较低，表明H⁺分泌存在缺陷。醛固酮缺乏的肾脏中，低于pH 6.0时的酸分泌（T.A.-pH 6.0），即远端肾单位H⁺分泌的指标，也显著降低。因此，醛固酮缺乏降低了远端肾单位的H⁺分泌能力，但对最大pH梯度所反映的泵的驱动力没有明显影响。将氨氯吡脒（10⁻⁵M）添加到进行H⁺分泌能力实验的肾脏灌注液中，以区分醛固酮的钠依赖性和非钠依赖性作用。在存在氨氯吡脒的情况下，醛固酮缺乏组和补充组肾脏之间T.A. pH 6.0的差异减少了约70%。这表明远端肾单位H⁺分泌的醛固酮依赖性成分的很大一部分是由钠依赖性机制介导的。
