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近端和远端肾单位对碳酸氢盐重吸收的增强维持了大鼠的低氯性代谢性碱中毒。

Augmented bicarbonate reabsorption by both the proximal and distal nephron maintains chloride-deplete metabolic alkalosis in rats.

作者信息

Wesson D E

机构信息

Veterans Administration Medical Center, Baylor College of Medicine, Houston, Texas 77211.

出版信息

J Clin Invest. 1989 Nov;84(5):1460-9. doi: 10.1172/JCI114321.

DOI:10.1172/JCI114321
PMID:2808701
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC304010/
Abstract

Whether augmented bicarbonate reabsorption by renal tubular epithelium contributes to the maintenance of chloride-deplete metabolic alkalosis is not clear. This study used free-flow micropuncture to investigate bicarbonate reabsorption by surface nephron segments in a rat model of diuretic-induced alkalosis compared to control. The proximal and distal nephron of the alkalotic animals had higher values for both delivered load to and absolute reabsorption from these segments. The proximal tubules of alkalotic and control animals had similar values for the slopes of the linear regression of delivered load vs. reabsorption and for the bicarbonate tubular fluid to plasma (TF/P) ratio at the late proximal tubule. By contrast, the corresponding analysis for the distal segment of alkalotic animals revealed a greater slope (0.98 vs. 0.81, P less than 0.003) and a smaller bicarbonate TF/P ratio at the late distal tubule (0.10 vs. 0.16, P less than 0.006). The data indicate that augmented bicarbonate reabsorption by both the proximal and distal nephron contributes to maintaining the alkalosis of this model. The data suggest primary stimulation of bicarbonate reabsorption in the distal nephron and load-dependent reabsorption in the proximal tubule.

摘要

肾小管上皮细胞增强的碳酸氢盐重吸收是否有助于维持低氯性代谢性碱中毒尚不清楚。本研究采用自由流微穿刺技术,与对照组相比,在利尿剂诱导的碱中毒大鼠模型中研究表层肾单位节段对碳酸氢盐的重吸收。碱中毒动物的近端和远端肾单位,这些节段的输送负荷和绝对重吸收值均较高。碱中毒动物和对照动物的近端小管,在输送负荷与重吸收的线性回归斜率以及近端小管后期的碳酸氢盐肾小管液与血浆(TF/P)比值方面具有相似的值。相比之下,碱中毒动物远端节段的相应分析显示,远端小管后期的斜率更大(0.98对0.81,P小于0.003),碳酸氢盐TF/P比值更小(0.10对0.16,P小于0.006)。数据表明,近端和远端肾单位增强的碳酸氢盐重吸收有助于维持该模型的碱中毒状态。数据提示远端肾单位碳酸氢盐重吸收的主要刺激以及近端小管中负荷依赖性重吸收。

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本文引用的文献

1
Dependency of proximal tubular fluid transport on the load of glomerular filtrate.近端肾小管液转运对肾小球滤过负荷的依赖性。
Kidney Int. 1981 Jul;20(1):18-28. doi: 10.1038/ki.1981.99.
2
Intracellular potential and K+ activity in rat kidney proximal tubular cells in acidosis and K+ depletion.酸中毒和钾缺乏时大鼠肾近端小管细胞的细胞内电位及钾活性
J Membr Biol. 1982;69(2):159-65. doi: 10.1007/BF01872275.
3
Metabolic alkalosis in the rat. Evidence that reduced glomerular filtration rather than enhanced tubular bicarbonate reabsorption is responsible for maintaining the alkalotic state.大鼠的代谢性碱中毒。有证据表明,维持碱中毒状态的原因是肾小球滤过率降低,而非肾小管对碳酸氢盐的重吸收增强。
J Clin Invest. 1983 May;71(5):1141-60. doi: 10.1172/jci110864.
4
Effects of extracellular fluid volume and plasma bicarbonate concentration on proximal acidification in the rat.细胞外液量和血浆碳酸氢盐浓度对大鼠近端酸化的影响。
J Clin Invest. 1983 Mar;71(3):736-46. doi: 10.1172/jci110821.
5
Correction of acute chloride-depletion alkalosis in the rat without volume expansion.大鼠急性氯耗竭性碱中毒的纠正而无容量扩张。
Am J Physiol. 1983 Feb;244(2):F217-21. doi: 10.1152/ajprenal.1983.244.2.F217.
6
Proximal tubular bicarbonate reabsorption and PCO2 in chronic metabolic alkalosis in the rat.大鼠慢性代谢性碱中毒时近端肾小管碳酸氢盐重吸收与二氧化碳分压
J Clin Invest. 1983 Oct;72(4):1385-95. doi: 10.1172/JCI111095.
7
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Am J Physiol. 1983 Oct;245(4):F478-84. doi: 10.1152/ajprenal.1983.245.4.F478.
8
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