Relationship between Sodium Intake and Water Intake: The False and the True

Background: Generally, eating salty food items increases thirst. Thirst is also stimulated by the experimental infusion of hypertonic saline. But, in steady state, does the kidney need a higher amount of water to excrete sodium on a high than on a low sodium intake? This issue is still controversial. The purpose of this review is to provide examples of how the kidney handles water in relation to salt intake/output. It is based on re-analysis of previously published studies in which salt intake was adjusted to several different levels in the same subjects, and in databases of epidemiologic studies in populations on an ad libitum diet. Summary and Key Messages: These re-analyses allow us to draw the following conclusions: (1) In a steady state situation, the urine volume (and thus the fluid intake) remains unchanged over a large range of sodium intakes. The adaptation to a higher sodium excretion rests only on changes in urinary sodium concentration. However, above a certain limit, this concentration cannot increase further and the urine volume may then increase. (2) In population studies, it is not legitimate to assume that sodium is responsible for changes in urine volume, since people who eat more sodium also eat more of other nutrients leading to an increase in the excretion of potassium, urea and other solutes, besides sodium. (3) After an abrupt increase in sodium intake, fluid intake is increased in the first few days, but urine volume does not change. The extra fluid drunk is responsible for an increase in body weight.

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Young Adults with Higher Salt Intake Have Inferior Hydration Status: A Cross-Sectional Study

Nutrients ◽

10.3390/nu14020287 ◽

2022 ◽

Vol 14 (2) ◽

pp. 287

Author(s):

Jianfen Zhang ◽

Na Zhang ◽

Shufang Liu ◽

Songming Du ◽

Guansheng Ma

Keyword(s):

Young Adults ◽

Water Intake ◽

Fluid Intake ◽

Salt Intake ◽

Sodium Intake ◽

Urine Specific Gravity ◽

Hydration Status ◽

Cross Sectional ◽

High Salt Intake ◽

Different Levels

The body’s water and sodium balances are tightly regulated and monitored by the brain. Few studies have explored the relationship between water and salt intake, and whether sodium intake with different levels of fluid intake leads to changes in hydration status remains unknown. The aim of the present study was to determine the patterns of water intake and hydration status among young adults with different levels of daily salt intakes. Participants’ total drinking fluids and water from food were determined by a 7-day 24-h fluid intake questionnaire for 7 days (from Day 1 to Day 7) and duplicate portion method (Day 5, Day 6 and Day 7). Urine of 24 h for 3 days (Day 5, Day 6 and Day 7) was collected and tested for the osmolality, the urine-specific gravity (USG), the concentrations of electrolytes, pH, creatinine, uric acid and the urea. The fasting blood samples for 1 day (Day 6) were collected and measured for the osmolality and the concentrations of electrolytes. The salt intakes of the participants were evaluated from the concentrations of Na of 24 h urine of 3 days (Day 5, Day 6 and Day 7). Participants were divided into four groups according to the quartile of salt intake, including the low salt intake (LS1), LS2, high salt intake (HS1) and HS2 groups. In total, 156 participants (including 80 male and 76 female young adults) completed the study. The salt intakes were 7.6, 10.9, 14.7 and 22.4 g among participants in the four groups (LS1, LS2, HS1 and HS2 groups, respectively), which differed significantly in all groups (F = 252.020; all p < 0.05). Compared to the LS1 and LS2 groups, the HS2 group had 310–381, 250–358 and 382–655 mL more amounts of water from the total water intake (TWI), total drinking fluids and water from food (all p < 0.05), respectively. Participants in the HS2 group had 384–403, 129–228 and 81–114 mL more in the water, water from dishes and staple foods, respectively, than those in the groups of LS1 and LS2 (p < 0.05). The HS2 group excreted 386–793 mL more urine than those in the groups of LS1 and LS2 (p < 0.05). However, regarding urine osmolality, the percentage of participants with optimal hydration status decreased from 41.0% in LS1 and LS2 to 25.6% in the HS2 group (p < 0.05). Participants with higher salt intake had higher TWI, total drinking fluids and water from food. Nevertheless, they had inferior hydration status. A reduction in salt intake should be encouraged among young adults to maintain optimal hydration status.

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CONSERVATIVE MANAGEMENT OF ACUTE RENAL FAILURE

PEDIATRICS ◽

10.1542/peds.25.3.409 ◽

1960 ◽

Vol 25 (3) ◽

pp. 409-418

Author(s):

S. A. Kaplan ◽

J. Strauss ◽

A. M. Yuceoglu

Keyword(s):

Renal Failure ◽

Acute Renal Failure ◽

Fluid Intake ◽

Sodium Intake ◽

Caloric Intake ◽

Urine Volume ◽

Proximal Tubules ◽

Cation Exchange Resins ◽

Exchange Resins ◽

Insensible Loss

The observations during treatment of three children with acute renal failure by a conservative regimen of therapy are presented. One patient died. The regimen has also been applied to six adults with renal failure; one died. The urine in the early stages of renal failure may be iso-osmotic with plasma and may represent unmodified fluid from the proximal tubules. Cardiac failure associated with hyperkalemia or administration of excessive quantities of fluids is the most frequent cause of death in this disorder. A regimen of therapy is described which embodies the following principles: a) Limitation of daily fluid intake to insensible loss plus the urine volume of the previous day. b) Restriction of sodium intake from the beginning to anticipate the development of acidosis. c) Use of cation exchange resins to prevent excessive increase in the concentration of potassium in the serum. d) Provision of adequate caloric intake through the administration of emulsified fat intravenously. e) Treatment of hyperphosphatemia and hypocalcemia when they occur. f) Continuation of careful supervision and therapy, even after the diuretic phase begins, since renal function continues to be severely restricted for several days afterwards.

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Abstract P614: Relationship Of Sodium Intake And Stress With Bone Health In Women

Hypertension ◽

10.1161/hyp.68.suppl_1.p614 ◽

2016 ◽

Vol 68 (suppl_1) ◽

Author(s):

Allison Jasti ◽

Deborah L Stewart ◽

Gregory A Harshfield

Keyword(s):

Bone Health ◽

Salt Intake ◽

Sodium Intake ◽

Target Organ Damage ◽

African American Adolescents ◽

Ang Ii ◽

Mineral Density ◽

High Sodium ◽

Low Sodium ◽

Relationship Of

Background: The skeleton is vital to sodium homeostasis, accounting for 40% of the body’s sodium. Research indicates stress and low sodium intake are independently associated with RAAS activation. In certain populations, stress can induce salt sensitivity, increasing the risk of hypertension and target organ damage, but the association of low versus high sodium intake with bone health is controversial. Purpose: This study sought out the relationship of low sodium and stress-induced RAAS activation with bone health. The tested hypothesis was those with lowest sodium intake would have lower total bone mineral density (TBMD) and content (TBMC) associated with stress-induced increases in angiotensin ii (Ang II) and aldosterone (Aldo). Methods: We compared effect of stress on Ang II, Aldo, TBMD and TMBC in healthy Caucasian and African-American adolescents. Subjects were grouped by quartiles based on sodium intake, assessed by urinary sodium excretion. Results: Due to females, overall significant inverse associations are observed between TBMD, TBMC, Ang II and Aldo in the lowest sodium intake quartile. Post-stress, women in the lowest sodium intake quartile showed that increases in both Ang II and Aldo correspond with lower TMBC and TMBD. There was no significance between Ang II, Aldo, TMBC and TMBD in the three highest quartiles of women nor in any male quartile. Conclusion: These data suggest Ang II and Aldo may reduce TMBC and TMBD in women. Stress-induced increases in Ang II and Aldo, with low sodium intake, may further reduce TBMD and TBMC in women. Ang II inhibition and/or moderated salt intake may be an efficacious prevention or treatment against the development of osteoporosis.

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Steady-state arterial pressure-urinary output relationships during ovine pregnancy

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1992.263.5.r1141 ◽

1992 ◽

Vol 263 (5) ◽

pp. R1141-R1146

Author(s):

E. W. Quillen ◽

B. S. Nuwayhid

Keyword(s):

Renal Function ◽

Steady State ◽

Arterial Pressure ◽

Sodium Intake ◽

Control Level ◽

Urine Volume ◽

Urinary Sodium Excretion ◽

Pregnant Sheep ◽

Plasma Angiotensin ◽

Steady State Levels

To determine the effects of long-term changes in sodium intake on mean arterial pressure (MAP) regulation during pregnancy, nonpregnant (n = 16) and 110- to 140-day pregnant (n = 13) ewes received total daily sodium intakes of 10, 30, 100, 400, and 1,200 mmol for 7 days. The sheep were housed in metabolism cages and MAP was monitored 24 h/day. Urinary sodium excretion (UNaV) followed changes in sodium intake, with steady-state levels being achieved with similar degrees of rapidity (2-3 days) in nonpregnant and pregnant sheep. At 10 mmol/day sodium intake, MAP was lower (79 +/- 1 vs. 82 +/- 2 mmHg; P < 0.01) and water intake (2,275 +/- 494 vs. 3,286 +/- 725 ml/day; P < 0.001) and 24-h urine volume (1,454 +/- 279 vs. 2,299 +/- 496 ml/day; P < 0.01) were greater in pregnant sheep. All of these variables exhibited direct relationships with increases in sodium intake. Plasma angiotensin II (pANG II) was increased in pregnancy (10.6 +/- 1.6 vs. 24.5 +/- 6.3 pg/ml; P < 0.001) at 10 mmol/day. Elevation of sodium intake suppressed pANG II to minimal levels in nonpregnant sheep, but to only 25% of the control level in pregnant sheep. During pregnancy, the renal function curve representing the steady-state MAP-UNaV relationship was shifted to lower MAP setpoint, but the sodium sensitivity of MAP was unchanged. Also, the inverse relationship of sodium intake and pANG II was blunted, suggesting a reduced role for ANG II in the maintenance of renal function during pregnancy.

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Repeated Exposure to Low-Sodium Cereal Affects Acceptance but Does not Shift Taste Preferences or Detection Thresholds of Children in a Randomized Clinical Trial

Journal of Nutrition ◽

10.1093/jn/nxz014 ◽

2019 ◽

Vol 149 (5) ◽

pp. 870-876 ◽

Cited By ~ 2

Author(s):

Nuala Bobowski ◽

Julie A Mennella

Keyword(s):

Repeated Measures ◽

Salt Intake ◽

Energy Content ◽

Sodium Intake ◽

Dietary Sodium ◽

Taste Preferences ◽

Detection Thresholds ◽

Salt Taste ◽

Low Sodium ◽

Secondary Outcomes

ABSTRACT Background Although salt taste preference is malleable in adults, no research to date has focused on children, whose dietary sodium intake exceeds recommended intake and whose salt taste preferences are elevated. Objective This proof-of-principle trial determined whether 8-wk exposure to low-sodium cereal (LSC) increased children's acceptance of its taste and changed their salty and sweet taste preferences. Methods Children (n = 39; ages 6–14 y; 67% female) were randomly assigned to ingest LSC or regular-sodium cereal (RSC) 4 times/wk for 8 wk. The cereals, similar in sugar (3 g/cup compared with 2 g/cup) and energy content (100 kcal/cup) yet different in sodium content (200 mg sodium/cup compared with 64 mg sodium/cup), were chosen based on taste evaluation by a panel of children. Mothers completed daily logs on children's cereal intake. At baseline and after the exposure period, taste tests determined which cereal children preferred and measured children's most preferred amount of salt (primary outcomes), and most preferred amount of sucrose and salt taste detection thresholds (secondary outcomes). Repeated measures ANOVAs were conducted on primary and secondary outcomes, and generalized estimating equations were conducted on amount of cereal ingested at home over time. Results Both treatment groups accepted and ate the assigned cereal throughout the 8-wk exposure. There were no group × time interactions in salt detection thresholds (P = 0.32) or amount of salt (P = 0.30) and sucrose (P = 0.77) most preferred, which were positively correlated (P = 0.001). At baseline and after the exposure, the majority in both groups preferred the taste of the RSC relative to LSC (P > 0.40). Conclusions Children showed no change in salt preference but readily ate the LSC for 8 consecutive weeks. Findings highlight the potential for reducing children's dietary salt intake by incorporating low-sodium foods in the home environment without more preferred higher-salt versions of these foods. This trial was registered at clinicaltrials.gov as NCT02909764.

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Regulation of angiotensin type 1 receptor and its gene expression: role in renal growth.

Journal of the American Society of Nephrology ◽

10.1681/asn.v82193 ◽

1997 ◽

Vol 8 (2) ◽

pp. 193-198

Author(s):

D H Wang ◽

Y Du ◽

H Zhao ◽

J P Granger ◽

R C Speth ◽

...

Keyword(s):

Salt Intake ◽

Sodium Intake ◽

Plasma Renin ◽

At1 Receptor ◽

Sodium Depletion ◽

Renal Growth ◽

Sodium Diet ◽

Low Sodium ◽

Low Salt ◽

Losartan Treatment

Low sodium intake has been demonstrated to upregulate the gene expression of the predominant renal type 1 angiotensin II (Ang II) receptor (AT1), the AT1A subtype. The study presented here tests the hypothesis that the upregulation of renal AT1 mRNA induced by sodium depletion occurs conjointly with an elevation of the AT1 receptor that modulates renal growth. Seven-week-old male Wistar rats were divided into four groups and treated for 2 wk with normal sodium diet, normal sodium diet plus 3 mg/kg/day losartan, low sodium diet, or low sodium diet plus losartan. Body weight and MAP were not significantly different among the four groups. Plasma renin activity was significantly elevated by losartan treatment, low salt intake, or a combination of the two, compared with the plasma renin activity of the controls. Northern blot analysis indicated that renal AT1 mRNA levels were significantly increased-183% by losartan, 212% by low salt intake, and 227% by the combination of the two-compared with their levels in controls. Radioligand binding assays revealed that AT1 receptors were significantly increased by low salt intake but were significantly decreased by losartan treatment. Renal AT1 receptor binding in the rats subjected to sodium depletion plus losartan did not differ from that in control rats. Kidney weight, kidney weight/body weight ratio, and renal DNA and protein content were not altered by sodium depletion but were significantly lowered by losartan treatment with both normal and low sodium intake, compared with those of controls. The protein/DNA ratio was not significantly different among the four groups. Blockade of renal AT1 receptors with losartan was found to retard normal renal growth, indicating that Ang II is required for normal renal development. Low sodium intake was found to increase mRNA and expression of the renal AT1 receptor but to have no effect on renal growth, suggesting that an increase in renal mass above a normal level requires the activation of multiple factors. Blockade of the AT1 receptor by losartan was found to upregulate AT1 mRNA but to down-regulate the AT1 receptor, suggesting that AT1 receptor-mediated intracellular events are necessary to sustain functional AT1 receptor expression in the kidney.

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Effect of Low Electrolyte Feeding on Development of Potassium Deficiency

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1957.191.3.610 ◽

1957 ◽

Vol 191 (3) ◽

pp. 610-614 ◽

Cited By ~ 7

Author(s):

Malcolm A. Holliday ◽

William E. Segar

Keyword(s):

Potassium Concentration ◽

Sodium Intake ◽

Extracellular Volume ◽

Sodium Concentration ◽

Potassium Deficiency ◽

Electrolyte Composition ◽

Urine Excretion ◽

Deficient Diet ◽

Sodium Potassium ◽

Low Sodium

Rats fed a diet deficient in sodium, potassium and chloride were observed for 3, 6, 12, 28, 60 and 110 days. Urine excretion of these ions was observed during the initial adjustment to the diet. Serum and muscle electrolyte composition was determined at the end of each interval. Initially the loss of sodium and chloride constituted a loss of extracellular volume without change in concentration. The loss of potassium in this period resulted in a decrease in the intracellular concentration of potassium. Subsequent conservation of all three substances was very effective. No alkalosis developed during the first 28 days on the deficient diet despite an 18% reduction in muscle potassium concentration. A minimal increase in muscle sodium concentration was observed at this level of potassium deficiency. Evidence indicates that this minimal increase was not a function of the low sodium intake per se but rather was characteristic of the magnitude of potassium deficiency, since a similar minimal increase in muscle sodium occurs when an adequate sodium intake is provided.

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Abstract 020: Physiological Significance of Angiotensin AT 1A Receptors in Vasopressin-producing Cells of the Supraoptic Nucleus

Hypertension ◽

10.1161/hyp.68.suppl_1.020 ◽

2016 ◽

Vol 68 (suppl_1) ◽

Author(s):

Danny W Linggonegoro ◽

Jeremy A Sandgren ◽

Kristin E Claflin ◽

Katherine J Perschbacher ◽

Jonathan Ni ◽

...

Keyword(s):

Fluid Intake ◽

Sodium Intake ◽

Urine Volume ◽

Renin Angiotensin System ◽

Normal Serum ◽

Serum Osmolality ◽

Angiotensin System ◽

Elevated Activity ◽

Bac Transgene ◽

The Brain

Low-renin and salt-sensitive forms of hypertension are characterized by elevated activity of the brain renin-angiotensin system and secretion of arginine vasopressin (AVP). While angiotensin in the brain is a known stimulant of AVP secretion through its AT 1 receptor, the localization of relevant AT 1 receptors remains unclear. We tested whether AT 1A receptors localized to AVP-producing cells are important for AVP secretion. To examine AVP and AT 1A co-localization, mice expressing Cre-recombinase via the AVP gene (AVP-Cre) were bred with mice expressing a conditional red fluorescent ROSA-stop flox -tdTomato construct and GFP via an AT 1A BAC transgene. Dual-fluorescent cells were detected in supraoptic nuclei (SON) but not paraventricular nuclei. Mice lacking AT 1A specifically in AVP-producing cells (AT 1A AVP-KO ) were then generated by breeding AVP-Cre mice with mice harboring a conditional endogenous AT 1A gene. AT 1A AVP-KO mice exhibited normal serum (littermate n=13, 353±69 vs AT 1A AVP-KO n=7, 207±37 pg/mL, p=NS) and urine (n=26, 145±33 vs n=11, 170±54 pg/mL, p=NS) copeptin (the stable C-terminal fragment of AVP) as well as hematocrit (n=14, 46.3±0.7 vs n=7, 47.5±1.3 %, p=NS) despite increased serum osmolality (n=33, 324±1.3 vs n=19, 330±1.6 mOsm/kg, p<0.01), supporting a role for AT 1A in AVP-producing cells in modulating the osmotic control of AVP release. Systolic blood pressure (SBP) (n=18, 109±1.3 vs n=5, 107±1.2 mmHg), urine volume (n=27, 1.1±0.1 vs n=12, 0.9±0.2 mL/d), and fluid intake (n=27, 4.0±0.2 vs n=12, 3.9±0.2 mL/d) were all normal (p=NS) in AT 1A AVP-KO mice. Two-bottle choice between water and escalating concentrations of NaCl uncovered minor alterations in sodium intake behavior. Serum osmolality (n=22, 336±2 vs n=9, 333±3 mOsm/kg), SBP (n=23, +10.4±2.1 vs n=8, +12.9±2.0 mmHg), urine output (n=23, +12.7±0.8 vs n=9, +12.7±1.5 g/day), and fluid intake (n=23, +16.2±1.3 vs n=9, +14.8±2.5 mL/day) all increased normally (p=NS) in response to deoxycorticosterone acetate (DOCA)-salt treatment. Collectively these data support a role for AT 1A receptors, localized specifically to AVP-expressing cells of the SON, in the normal osmotic control of AVP secretion.

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Renal nerve effects on renal adaptation to changes in sodium intake during ovine pregnancy

AJP Renal Physiology ◽

10.1152/ajprenal.1992.262.5.f823 ◽

1992 ◽

Vol 262 (5) ◽

pp. F823-F829

Author(s):

G. W. Aberdeen ◽

S. C. Cha ◽

S. Mukaddam-Daher ◽

B. S. Nuwayhid ◽

E. W. Quillen

Keyword(s):

Steady State ◽

Sodium Intake ◽

Urinary Sodium Excretion ◽

Renal Nerves ◽

Renal Nerve ◽

High Sodium ◽

Low Sodium ◽

Pregnant Sheep ◽

Urinary Potassium ◽

Renal Nerve Activity

To assess the possibility of an enhanced role of renal nerves in the control of urinary sodium excretion (UNaV) and fluid homeostasis during pregnancy, urine output, UNaV, and urinary potassium excretion were assessed hourly for 3 days before and for 6 days after a step reduction in total daily sodium intake from 400 to 40 mmol. Studies were performed in normal conscious sheep (4 nonpregnant and 4 pregnant). Each animal was prepared with a divided bladder so that urine could be collected simultaneously from one normally innervated and one denervated kidney. In nonpregnant ewes, ratios of the rates of excretion by denervated vs. innervated kidneys for UNaV averaged 1.00 +/- 0.07 under steady-state conditions at high levels of sodium intake. This ratio was not different at the low-sodium-intake state. In contrast, this ratio was 1.15 +/- 0.07 at high sodium intake and 1.13 +/- 0.03 at low sodium intake in pregnant ewes. The ratios at both steady-state intake levels were different (P less than 0.05) between nonpregnant and pregnant sheep. During the transition between sodium intake states, these ratios were unchanged in nonpregnant animals, whereas pregnant animals exhibited peak ratios of 2.20 +/- 0.39 (P less than 0.05), indicating sodium wasting by the denervated kidneys. In summary, the data suggest that renal nerve activity may not be completely suppressed by high sodium intakes in pregnant sheep. Furthermore, the renal nerves have an enhanced influence on sodium conservation during and after the transition from high- to low-sodium-intake states during pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)

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Dissociation between uric acid and urea clearances in the syndrome of inappropriate secretion of antidiuretic hormone related to salt excretion

Clinical Science ◽

10.1042/cs0780451 ◽

1990 ◽

Vol 78 (5) ◽

pp. 451-455 ◽

Cited By ~ 17

Author(s):

G. Decaux ◽

F. Prospert ◽

P. Cauchie ◽

A. Soupart

Keyword(s):

Uric Acid ◽

Antidiuretic Hormone ◽

Sodium Excretion ◽

Salt Intake ◽

Sodium Intake ◽

Fractional Excretion ◽

Urinary Sodium Excretion ◽

Low Sodium ◽

Inappropriate Secretion ◽

Salt Excretion

1. Our purpose was to determine why hypouricaemia is more frequently observed than hypouraemia in the syndrome of inappropriate secretion of antidiuretic hormone. We have retrospectively analysed the scores of 35 patients with a chronic form of hyponatraemia related to the syndrome of inappropriate secretion of antidiuretic hormone and studied prospectively six patients. 2. The patients with high fractional excretion of filtered urea (>55%) presented lower blood urea and lower salt excretion than the patients with normal fractional excretion of filtered urea, despite similar levels of hyponatraemia and of osmotic and uric acid clearances. In six hyponatraemic patients, an increase in salt intake was accompanied by a decrease in fractional excretion of filtered urea. In the syndrome of inappropriate secretion of antidiuretic hormone, the fractional excretion of filtered urea was inversely correlated to the fractional excretion of filtered sodium (r = −0.66; P <0.001), whereas the fractional excretion of filtered uric acid was not dependent on sodium excretion. 3. Hypouraemia with high fractional excretion of filtered urea in patients with the syndrome of inappropriate secretion of antidiuretic hormone is related to low urinary sodium excretion and thus reflects low sodium intake.

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