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New roles for chloride in renal physiology and pathophysiology.

作者信息

Luke R G, Gifford J D, Galla J H

机构信息

Department of Internal Medicine, University of Cincinnati Medical Center, Ohio.

出版信息

Trans Am Clin Climatol Assoc. 1991;102:84-93; discussion 93-5.

PMID:2130571
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2376645/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49f1/2376645/d22971c81e55/tacca00086-0164-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49f1/2376645/d22971c81e55/tacca00086-0164-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49f1/2376645/d22971c81e55/tacca00086-0164-a.jpg

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New roles for chloride in renal physiology and pathophysiology.氯离子在肾脏生理和病理生理中的新作用。
Trans Am Clin Climatol Assoc. 1991;102:84-93; discussion 93-5.
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引用本文的文献

1
"I don't get no respect": the role of chloride in acute kidney injury.“我得不到尊重”：氯离子在急性肾损伤中的作用。
Am J Physiol Renal Physiol. 2019 Mar 1;316(3):F587-F605. doi: 10.1152/ajprenal.00130.2018. Epub 2018 Dec 12.

本文引用的文献

1
Mineralocorticoid-resistant renal hyperkalemia without salt wasting (type II pseudohypoaldosteronism): role of increased renal chloride reabsorption.无盐耗竭的盐皮质激素抵抗性肾性高钾血症（II型假性醛固酮增多症）：肾氯重吸收增加的作用
Kidney Int. 1981 May;19(5):716-27. doi: 10.1038/ki.1981.72.
2
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.
3
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.
4
Segmental chloride and fluid handling during correction of chloride-depletion alkalosis without volume expansion in the rat.大鼠在纠正无容量扩张的氯耗竭性碱中毒过程中的节段性氯和液体处理
J Clin Invest. 1984 Jan;73(1):96-106. doi: 10.1172/JCI111211.
5
Volume-independent reductions in glomerular filtration rate in acute chloride-depletion alkalosis in the rat. Evidence for mediation by tubuloglomerular feedback.大鼠急性氯耗竭性碱中毒时肾小球滤过率的容量非依赖性降低。管球反馈介导的证据。
J Clin Invest. 1984 Dec;74(6):2002-8. doi: 10.1172/JCI111622.
6
Chloride-depletion alkalosis with a normal extracellular fluid volume.伴有正常细胞外液量的低氯性碱中毒
Am J Physiol. 1983 Oct;245(4):F419-24. doi: 10.1152/ajprenal.1983.245.4.F419.
7
The response of normal man to selective depletion of hydrochloric acid. Factors in the genesis of persistent gastric alkalosis.
Am J Med. 1966 Jan;40(1):10-8. doi: 10.1016/0002-9343(66)90182-3.
8
Correction of metabolic alkalosis in man without repair of potassium deficiency. A re-evaluation of the role of potassium.在未纠正钾缺乏的情况下纠正人体代谢性碱中毒。对钾作用的重新评估。
Am J Med. 1966 Jan;40(1):19-26. doi: 10.1016/0002-9343(66)90183-5.
9
Correction of metabolic alkalosis by the kidney after isomertric expansion of extracellular fluid.细胞外液等容性扩张后肾脏对代谢性碱中毒的纠正。
J Clin Invest. 1968 May;47(5):1181-92. doi: 10.1172/JCI105807.
10
Bicarbonate transport by isolated perfused rat collecting ducts.分离灌注大鼠集合管的碳酸氢盐转运
Am J Physiol. 1985 Oct;249(4 Pt 2):F485-9. doi: 10.1152/ajprenal.1985.249.4.F485.