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长期钾调节分析

Analysis of long-term potassium regulation.

作者信息

Young D B

出版信息

Endocr Rev. 1985 Winter;6(1):24-44. doi: 10.1210/edrv-6-1-24.

DOI:10.1210/edrv-6-1-24
PMID:3884328
Abstract

Potassium regulation is maintained by a system which affects the rate of renal excretion of the ion and its distribution between the intra- and extracellular spaces. Long-term regulation is accomplished by the interactions of several components of the control system. The direct effect of changes in plasma potassium concentration on potassium secretion by the cells of the distal nephron is the most powerful regulator of K excretion. Changes in aldosterone concentration interact multiplicatively with the effect of plasma K on K excretion, and changes in aldosterone also affect the distribution of the ion so that elevations in aldosterone shift a greater proportion of K into the cells of the body. Sodium intake affects K excretion, increases in intake resulting in a higher rate of K excretion. Aldosterone secretion is regulated by a multiplicative interaction between angiotensin II and potassium concentration. An hypothesis that states in essence that long-term K regulation is determined by the interaction of several component systems is developed. A mathematical model constructed from the hypothesis employing data from experiments designed to quantitatively analyze the functions of the individual components is presented. The model is used to test the hypothesis by comparing the operation of the model with the results of experiments in which the potassium control system is subjected to a wide range of challenges and perturbations. General agreement between model predictions and experimental results was obtained, thereby providing support for the validity of the hypothesis. Building the model drew attention to several areas in which experimental investigation is required to obtain understanding of several important physiological processes. Finally, several predictions obtained from the model may have clinical relevance in the areas of renal medicine and hypertension.

摘要

钾的调节由一个系统维持,该系统影响离子的肾脏排泄速率及其在细胞内和细胞外空间之间的分布。长期调节是通过控制系统的几个组成部分的相互作用来实现的。血浆钾浓度变化对远端肾单位细胞钾分泌的直接影响是钾排泄最有力的调节因素。醛固酮浓度的变化与血浆钾对钾排泄的影响呈倍增相互作用,醛固酮的变化也影响离子的分布,因此醛固酮升高会使更大比例的钾转移到身体细胞中。钠摄入量影响钾排泄,摄入量增加导致钾排泄率升高。醛固酮分泌受血管紧张素II与钾浓度之间的倍增相互作用调节。提出了一种本质上认为长期钾调节由几个组成系统的相互作用决定的假说。给出了一个基于该假说构建的数学模型,该模型采用了旨在定量分析各个组成部分功能的实验数据。通过将模型的运行与钾控制系统受到广泛挑战和扰动的实验结果进行比较,该模型用于检验该假说。模型预测与实验结果总体一致,从而为该假说的有效性提供了支持。构建该模型使人们关注到几个需要进行实验研究以了解几个重要生理过程的领域。最后,从该模型获得的几个预测可能在肾脏病学和高血压领域具有临床相关性。

相似文献

1
Analysis of long-term potassium regulation.长期钾调节分析
Endocr Rev. 1985 Winter;6(1):24-44. doi: 10.1210/edrv-6-1-24.
2
Effects of sodium intake on steady-state potassium excretion.钠摄入对稳态钾排泄的影响。
Am J Physiol. 1984 Jun;246(6 Pt 2):F772-8. doi: 10.1152/ajprenal.1984.246.6.F772.
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Chronobiology of the renin-angiotensin-aldosterone system in dogs: relation to blood pressure and renal physiology.狗的肾素-血管紧张素-醛固酮系统的生物钟:与血压和肾功能的关系。
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Interaction between the natriuretic effects of renal perfusion pressure and the antinatriuretic effects of angiotensin and aldosterone in control of sodium excretion.肾灌注压的利钠作用与血管紧张素和醛固酮的抗利钠作用在钠排泄控制中的相互作用。
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Effects of sodium intake on plasma potassium and renin angiotensin aldosterone system in conscious dogs.钠摄入量对清醒犬血浆钾及肾素-血管紧张素-醛固酮系统的影响
Acta Physiol Scand. 2005 Jul;184(3):225-34. doi: 10.1111/j.1365-201X.2005.01452.x.
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Effect of sodium concentration on aldosterone secretion by isolated perfused canine adrenal glands.钠浓度对离体灌注犬肾上腺醛固酮分泌的影响。
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A mathematical model of potassium homeostasis: Effect of feedforward and feedback controls.钾离子稳态的数学模型:前馈和反馈控制的影响。
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Angiotensin II and renal excretion of sodium and potassium in unanaesthetized dogs.血管紧张素II与未麻醉犬的钠钾肾排泄
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2
Aldosterone: Renal Action and Physiological Effects.醛固酮:肾脏作用和生理效应。
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3
Direct and Indirect Mineralocorticoid Effects Determine Distal Salt Transport.
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Unique chloride-sensing properties of WNK4 permit the distal nephron to modulate potassium homeostasis.WNK4独特的氯离子感知特性使远端肾单位能够调节钾稳态。
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Evidence for a gastrointestinal-renal kaliuretic signaling axis in humans.人类胃肠道-肾脏排钾信号轴的证据。
Kidney Int. 2015 Dec;88(6):1383-1391. doi: 10.1038/ki.2015.243. Epub 2015 Aug 26.
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Serum potassium and cardiovascular mortality.血清钾与心血管死亡率。
J Gen Intern Med. 2000 Dec;15(12):885-90. doi: 10.1046/j.1525-1497.2000.91021.x.
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Angiotensin-independent mechanism for aldosterone synthesis during chronic extracellular fluid volume depletion.慢性细胞外液容量耗竭期间醛固酮合成的不依赖血管紧张素机制。
J Clin Invest. 1997 Mar 1;99(5):855-60. doi: 10.1172/JCI119249.
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Water deprivation: effects on fluid and electrolyte handling and plasma biochemistry in Long-Evans and Brattleboro rats.水分剥夺:对长 Evans 大鼠和布拉德福德大鼠的液体和电解质处理以及血浆生物化学的影响。
J Physiol. 1987 Apr;385:35-48. doi: 10.1113/jphysiol.1987.sp016482.