The body controls of salt and water balance: the
complex interplay of mechanisms has important
effects on hormones, metabolism, and possibly
development of disease.
Sodium chloride, commonly called dietary salt, is
essential to our body, but a high salt intake can
raise blood pressure, which can damage the body in
many ways over time.
High blood pressure has been linked to heart
disease, stroke, kidney failure, and other health
problems. However, not everyone is equally sensitive
to high levels of salt.
Researchers have long believed that the way the
level of salt inside our bodies is controlled is
fairly straightforward: when levels are too high,
our brains are stimulated to make us thirsty.
We drink more and excrete more urine, through which
the body expels excess salt.
To gain insight into this process, a team led by Dr.
Jens Titze at the University of Erlangen-Nuremberg
in Germany took the opportunity to study men
participating in a simulated space flight program.
Between 2009 and 2011, they tightly controlled the
daily salt intake of 10 men simulating a flight to
Mars: four in a 105-day pre-flight phase and six
others for 205 days.
The men were given 12 grams of salt per day, 9
g/day, or 6 g/day for 30–60 days.
The researchers collected all the men’s urine for
The scientists were surprised to find that, whatever
the level of salt consumed, sodium was stored and
released from the men’s bodies in roughly weekly and
The team uncovered similar rhythms for the hormones
aldosterone, which regulates sodium excretion from
the kidney, and glucocorticoids, which help regulate
Titze, now at Vanderbilt University Medical Center,
continued to examine the long-term control of sodium
and water balance in the men.
To better understand the mechanisms at work, his
team also performed experiments in mice.
Changing salt intake affected levels of both
aldosterone and glucocorticoids, the hormones found
to rhythmically control the body’s salt and water
These, in turn, had a number of interesting effects
in the body.
Increasing salt intake increased sodium excretion,
but also unexpectedly caused the kidney to conserve
Excess sodium was thus released in concentrated
This method of protecting the body’s water was so
efficient that the men actually drank less when
their salt intake was highest.
These results show that the body regulates its salt
and water balance not only by releasing excess
sodium in urine, but by actively retaining or
releasing water in urine.
The advantage of this mechanism is that the
long-term maintenance of body fluids isn’t as
dependent on external water sources as once
The researchers found that the kidney conserves or
releases water by balancing levels of sodium,
potassium, and the waste product urea.
This may be what ties glucocorticoid levels to salt
A high salt diet increased glucocorticoid levels,
causing muscle and liver to burn more energy to
produce urea, which was then used in the kidney for
That also led the mice to eat more.
These salt-driven changes in metabolism may thus
partly explain why high salt diets have been linked
to diabetes, heart disease, and other health
problems that can result from the condition known as
“We have always focused on the role of salt in
arterial hypertension. Our findings suggest that
there is much more to know—a high salt intake may
predispose to metabolic syndrome,” Titze says.
For more information
Increased salt consumption induces body water
conservation and decreases fluid intake. Rakova N,
Kitada K, Lerchl K, Dahlmann A, Birukov A, Daub S,
Kopp C, Pedchenko T, Zhang Y, Beck L, Johannes B,
Marton A, Müller DN, Rauh M, Luft FC, Titze J. J
Clin Invest. 2017 May 1;127(5):1932-1943. doi:
10.1172/JCI88530. Epub 2017 Apr 17. PMID: 28414302.
High salt intake reprioritizes osmolyte and energy
metabolism for body fluid conservation. Kitada K,
Daub S, Zhang Y, Klein JD, Nakano D, Pedchenko T,
Lantier L, LaRocque LM, Marton A, Neubert P,
Schröder A, Rakova N, Jantsch J, Dikalova AE,
Dikalov SI, Harrison DG, Müller DN, Nishiyama A,
Rauh M, Harris RC, Luft FC, Wassermann DH, Sands JM,
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doi: 10.1172/JCI88532. Epub 2017 Apr 17. PMID: