Mechanism of potassium depletion during chronic metabolic acidosis in the rat.
Mechanism of potassium depletion during chronic metabolic acidosis in the rat.
复制标题
大鼠慢性代谢性酸中毒期间钾消耗的机制。
DOI：
10.1152/ajprenal.1987.252.1.f122
复制
发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Ornt,DB
中科院分区：
文献类型：
--
作者：
Scandling,JD;Ornt,DB
对正常钾饮食的大鼠给予1.5%NH4Cl或水4天。酸喂养的动物出现代谢性酸中毒、负钾平衡和钾耗竭。尿钠排泄量和尿流量在第一天之后在组间没有差异。4天后，在正常pH和碳酸氢盐浓度下灌注来自这些组中的每一组中的动物的离体肾脏。尽管在酸喂养动物中存在钾耗竭，但两组之间的尿钾排泄量相似。相比之下，来自具有由饮食钾限制诱导的相当的钾耗竭的动物的分离的肾脏容易保存钾（排泄分数0.35 +/- 0.04 vs. 0.83 +/- 0.09，来自酸喂养动物的肾脏，P小于0.01）。三组离体肾脏的钠排泄和尿流量相似。在摄入NH 4Cl 4天后，酸喂养大鼠的血浆醛固酮浓度高于对照动物（43 +/- 10 vs. 10 +/- 2 ng/dl，P <0.01）。切除肾上腺的大鼠用正常（4微克/天）或高（22微克/天）的醛固酮替代治疗，同时摄入氯化铵4天。只有在高醛固酮替代的存在下，酸喂养的肾上腺切除动物才出现钾耗竭。我们的结论是，慢性代谢性酸中毒刺激醛固酮分泌，醛固酮维持不适当的高尿钾排泄和钾耗竭，在这种酸碱平衡紊乱。
Pair-fed rats on a normal K diet were given either 1.5% NH4Cl or water for 4 days. The acid-fed animals developed metabolic acidosis, negative K balance, and K depletion. Urinary Na excretion and urinary flow were not different between the groups beyond the first day. After the 4 days, isolated kidneys from animals in each of these groups were perfused at normal pH and bicarbonate concentrations. Urinary K excretion was similar between the groups despite the potassium depletion in the acid-fed animals. In contrast, isolated kidneys from animals with comparable K depletion induced by dietary K restriction readily conserved K (fractional excretion 0.35 +/- 0.04 vs. 0.83 +/- 0.09 by the kidneys from acid-fed animals, P less than 0.01). Sodium excretion and urinary flow were similar among the three groups of isolated kidneys. Plasma aldosterone concentrations were greater in the acid-fed rats after the 4 days of NH4Cl ingestion than in the control animals (43 +/- 10 vs. 10 +/- 2 ng/dl, P less than 0.01). Adrenalectomized rats were treated with either normal (4 micrograms/day) or high (22 micrograms/day) aldosterone replacement while ingesting NH4Cl for 4 days. Only in the presence of high aldosterone replacement did the acid-fed adrenalectomized animals develop K depletion. We conclude that chronic metabolic acidosis stimulates aldosterone secretion, and that aldosterone maintains the inappropriately high urinary potassium excretion and K depletion seen in this acid-base disorder.