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抗利尿激素-渴觉反馈机制对细胞外钠浓度的调控

Control of extracellular sodium concentration by antidiuretic hormone-thirst feedback mechanism.

作者信息

Young D B, Pan Y J, Guyton A C

出版信息

Am J Physiol. 1977 May;232(5):R145-9. doi: 10.1152/ajpregu.1977.232.5.R145.

Abstract

The effectiveness of the antidiuretic hormone (ADH)-thirst feedback mechanism to control extracellular sodium concentration was studied in dogs. The design consisted of increasing daily sodium intake from 10 to 200 meq in a group of dogs, first in the normal condition and second with a continuous 24 h/day infusion of an amount of ADH sufficient to maintain urine osmolarity at a maximal level and with fixed water intake. We were therefore able to compare the effectiveness of sodium concentration control in the same dogs with and without feedback control of the ADH-thirst mechanism, the difference in effectiveness being a quantitative measure of the control capability of the system. In the normal condition the increase in sodium intake resulted in a steady-state 2.3% elevation in sodium concentration. With the feedback control of ADH secretion and water intake blocked, the same sodium forcing produced an 11.9% increase in extracellular sodium concentration. The minimum feedback gain for the system calculated from the data is -4.2. We conclude that control of sodium concentration in the intact state is accomplished mainly by the ADH-thirst feedback mechanism.

摘要

在犬类中研究了抗利尿激素(ADH)-口渴反馈机制对控制细胞外钠浓度的有效性。实验设计包括在一组犬类中,首先在正常状态下,然后在每天24小时持续输注足以将尿渗透压维持在最高水平且固定水摄入量的ADH的情况下,将每日钠摄入量从10毫当量增加到200毫当量。因此,我们能够比较同一组犬类在有和没有ADH-口渴机制反馈控制的情况下控制钠浓度的有效性,有效性的差异是该系统控制能力的定量指标。在正常状态下,钠摄入量的增加导致钠浓度稳态升高2.3%。在ADH分泌和水摄入的反馈控制被阻断的情况下,相同的钠负荷使细胞外钠浓度增加了11.9%。根据这些数据计算出的该系统的最小反馈增益为-4.2。我们得出结论,在完整状态下,钠浓度的控制主要通过ADH-口渴反馈机制来实现。

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