Kornandakieti C, Tannen R L
J Lab Clin Med. 1984 Sep;104(3):293-303.
The effect of K+ homeostasis on distal nephron acidification was investigated by comparing isolated perfused kidneys from rats fed a K+-free or high-K+ diet for 1 week. H+ secretary capacity of the distal nephron was determined by perfusion of kidneys at pH 6.8 and providing saturating quantities of urinary buffer in the form of creatinine. Under these conditions, kidneys from rats with depleted K+ had a lower urine pH level and a higher excretion rate of titratable acid. Acid secretion below a pH of 6.0, an index of H+ secretion by the distal nephron, was also significantly greater in the rats with depleted K+. After addition of 10(-5) mol/L amiloride hydrochloride to the perfusate, urine pH levels remained lower and acid secretion below a pH of 6.0 remained higher in the group with low compared with high dietary K+. Thus, K+ depletion increases the intrinsic distal nephron H+ secretory capacity, and the mechanism appears to be independent of distal nephron Na+ transport. Additional comparisons with kidneys from control rats and rats with long-term metabolic acidosis and alkalosis suggest that the predominant effect on acidification is stimulation by K+ depletion rather than suppression by a high K+ intake. Because our data suggest that K+ depletion per se stimulates the distal nephron H+ transport system, it seems likely that the high urine pH level that accompanies K+ depletion in vivo is attributable entirely to the K+ depletion-induced increase in the rate of renal NH3 production.
通过比较用低钾或高钾饮食喂养1周的大鼠的离体灌注肾脏，研究了钾离子稳态对远端肾单位酸化的影响。远端肾单位的氢离子分泌能力通过在pH 6.8下灌注肾脏并以肌酐形式提供饱和量的尿缓冲剂来测定。在这些条件下，低钾大鼠的肾脏尿pH值较低，可滴定酸排泄率较高。低钾大鼠远端肾单位氢离子分泌指标（pH低于6.0时的酸分泌）也显著更高。向灌注液中加入10^(-5)mol/L盐酸阿米洛利后，低钾饮食组的尿pH值仍较低，pH低于6.0时的酸分泌仍较高。因此，低钾会增加远端肾单位固有的氢离子分泌能力，其机制似乎与远端肾单位钠离子转运无关。与对照大鼠以及长期代谢性酸中毒和碱中毒大鼠的肾脏进行的额外比较表明，对酸化的主要影响是低钾刺激而非高钾摄入抑制。因为我们的数据表明低钾本身会刺激远端肾单位的氢离子转运系统，所以体内低钾时伴随的高尿pH值似乎完全归因于低钾诱导的肾脏氨生成速率增加。
