Increased salt consumption induces body water conservation and decreases fluid intake
Natalia Rakova, … , Friedrich C. Luft, Jens Titze
Natalia Rakova, … , Friedrich C. Luft, Jens Titze
Published April 17, 2017
Citation Information: J Clin Invest. 2017;127(5):1932-1943. https://doi.org/10.1172/JCI88530.
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Clinical Research and Public Health Metabolism Nephrology

Increased salt consumption induces body water conservation and decreases fluid intake

Abstract

BACKGROUND. The idea that increasing salt intake increases drinking and urine volume is widely accepted. We tested the hypothesis that an increase in salt intake of 6 g/d would change fluid balance in men living under ultra-long-term controlled conditions.

METHODS. Over the course of 2 separate space flight simulation studies of 105 and 205 days’ duration, we exposed 10 healthy men to 3 salt intake levels (12, 9, or 6 g/d). All other nutrients were maintained constant. We studied the effect of salt-driven changes in mineralocorticoid and glucocorticoid urinary excretion on day-to-day osmolyte and water balance.

RESULTS. A 6-g/d increase in salt intake increased urine osmolyte excretion, but reduced free-water clearance, indicating endogenous free water accrual by urine concentration. The resulting endogenous water surplus reduced fluid intake at the 12-g/d salt intake level. Across all 3 levels of salt intake, half-weekly and weekly rhythmical mineralocorticoid release promoted free water reabsorption via the renal concentration mechanism. Mineralocorticoid-coupled increases in free water reabsorption were counterbalanced by rhythmical glucocorticoid release, with excretion of endogenous osmolyte and water surplus by relative urine dilution. A 6-g/d increase in salt intake decreased the level of rhythmical mineralocorticoid release and elevated rhythmical glucocorticoid release. The projected effect of salt-driven hormone rhythm modulation corresponded well with the measured decrease in water intake and an increase in urine volume with surplus osmolyte excretion.

CONCLUSION. Humans regulate osmolyte and water balance by rhythmical mineralocorticoid and glucocorticoid release, endogenous accrual of surplus body water, and precise surplus excretion.

FUNDING. Federal Ministry for Economics and Technology/DLR; the Interdisciplinary Centre for Clinical Research; the NIH; the American Heart Association (AHA); the Renal Research Institute; and the TOYOBO Biotechnology Foundation. Food products were donated by APETITO, Coppenrath und Wiese, ENERVIT, HIPP, Katadyn, Kellogg, Molda, and Unilever.

Authors

Natalia Rakova, Kento Kitada, Kathrin Lerchl, Anke Dahlmann, Anna Birukov, Steffen Daub, Christoph Kopp, Tetyana Pedchenko, Yahua Zhang, Luis Beck, Bernd Johannes, Adriana Marton, Dominik N. Müller, Manfred Rauh, Friedrich C. Luft, Jens Titze

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Figure 5

Long-term rhythmical hormonal control of water balance and its modulation by dietary salt intake.

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Long-term rhythmical hormonal control of water balance and its modulatio...
(A) Effect of rhythmical mineralocorticoid release, independent of salt intake, on water intake (n = 1,646), urine volume (n = 1,644), renal water balance (n = 1,646), and body weight (n = 1,631). (B) Effect of rhythmical glucocorticoid release, independent of salt intake, on water intake (n = 1,646), urine volume (n = 1,644), renal water balance (n = 1,646), and body weight (n = 1,631). (C) Projected combined effect of salt-driven modulation of rhythmical mineralocorticoid and glucocorticoid release on water intake, urine volume, renal water balance, and body weight. (D) Measured effect of third tertile Na+ excretion in the urine on water intake (n = 1,646), urine volume (n = 1,644), renal water balance (n = 1,646), and body weight (n = 1,631). Data were statistically analyzed by mixed linear model and are expressed as the Δ change ± SEM (A, B, and D). The projected combined effect of mineralocorticoid suppression and glucocorticoid increase by dietary salt intake in C was calculated from the data presented in A and B and the measured suppression of mineralocorticoid and increase in glucocorticoid levels by a 6-g/d increase in salt intake. Details on the supplemental calculations and statistical analyses pertaining to Figure 5 are provided in the Supplemental Materials (pages 22 and 148, respectively).