Response of renal NH3 production to chronic respiratory acidosis.
Response of renal NH3 production to chronic respiratory acidosis.
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肾脏 NH3 生成对慢性呼吸性酸中毒的反应。
DOI：
10.1152/ajprenal.1984.247.6.f896
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Tannen,RL
中科院分区：
文献类型：
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作者：
Rodriguez-Nichols,F;Laughrey,E;Tannen,RL
尽管慢性代谢性酸中毒会导致肾脏产生 NH3 的能力适应性增加，但对慢性呼吸性酸中毒产生的低 pH 值的反应尚不清楚。大鼠被放置在一个环境 CO2 为 10% 的特殊建造的房间中 3 天，这使得它们的 PCO2 增加到 76 +/- 4 mmHg。使用灌注有 0.5 mM 谷氨酰胺的分离肾脏和用 1 mM 谷氨酰胺孵育的皮质小管在体外测定 NH3 产量。患有慢性呼吸系统和慢性代谢性酸中毒的清醒大鼠具有相似的动脉pH值（7.29+/-0.01和7.31+/-0.01），显着低于对照组（7.41+/-0.04）。在 pH 7.4 下灌注的慢性呼吸性酸中毒大鼠的肾脏产生的 NH3 与正常对照没有显着差异（1.13 +/- 0.13 与 1.07 +/- 0.17 mumol X min-1 X g-1）。相比之下，慢性代谢性酸中毒大鼠的肾脏产生的 NH3 明显多于这两组大鼠 (2.73 +/- 0.29 mumol X min-1 X g-1)。与对照组相比，慢性呼吸性酸中毒大鼠的皮质小管也没有显示出 NH3（8.8 +/- 0.8 对比 11.6 +/- 0.8 mumol X min-1 X g-1）和葡萄糖（1.38 +/- 0.08 对比 1.41 +/- 0.13 mumol X min-1 X g-1）产生适应的证据，而慢性代谢性酸中毒刺激氨生成和氨生成。糖异生两倍或更多。因此，较低的全身 pH 值并不能解释肾脏产生氨或葡萄糖的能力的适应。（摘要截断为 250 字）
Although chronic metabolic acidosis results in an adaptive increase in the renal capacity to produce NH3, the response to a low pH produced by chronic respiratory acidosis is unknown. Rats were placed in a specially constructed chamber with an ambient CO2 of 10% for 3 days, which increased their PCO2 to 76 +/- 4 mmHg. NH3 production was determined in vitro using both isolated kidneys perfused with 0.5 mM glutamine and cortical tubules incubated with 1 mM glutamine. Conscious rats with chronic respiratory and chronic metabolic acidosis had similar arterial pHs (7.29 +/- 0.01 and 7.31 +/- 0.01), which were significantly lower than controls (7.41 +/- 0.04). NH3 production by kidneys from rats with chronic respiratory acidosis perfused at pH 7.4 did not differ significantly from normal controls (1.13 +/- 0.13 vs. 1.07 +/- 0.17 mumol X min-1 X g-1). By contrast, kidneys from rats with chronic metabolic acidosis produced significantly more NH3 than both these groups (2.73 +/- 0.29 mumol X min-1 X g-1). Cortical tubules from rats with chronic respiratory acidosis also showed no evidence of adaptation in both NH3 (8.8 +/- 0.8 vs. 11.6 +/- 0.8 mumol X min-1 X g-1) and glucose (1.38 +/- 0.08 vs. 1.41 +/- 0.13 mumol X min-1 X g-1) production in comparison with controls, whereas chronic metabolic acidosis stimulated both ammoniagenesis and gluconeogenesis twofold or more. Thus a low systemic pH does not account for the adaptation in the capacity of the kidney to produce either ammonia or glucose.(ABSTRACT TRUNCATED AT 250 WORDS)