Journal articles: 'Sodium in the body'

1

Simpson, F. O. "SODIUM INTAKE, BODY SODIUM, AND SODIUM EXCRETION." Lancet 332, no. 8601 (July 1988): 25–29. http://dx.doi.org/10.1016/s0140-6736(88)92954-6.

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Skøtt, Ole. "Body sodium and volume homeostasis." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 285, no. 1 (July 2003): R14—R18. http://dx.doi.org/10.1152/ajpregu.00100.2003.

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Simpson, F. O. "Sodium Intake, Sodium Handling and Body Sodium in Rats with Spontaneous Genetic Hypertension." Japanese Heart Journal 34, no. 4 (1993): 472–73. http://dx.doi.org/10.1536/ihj.34.472.

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Bie, Peter. "Mechanisms of sodium balance: total body sodium, surrogate variables, and renal sodium excretion." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 315, no. 5 (November 1, 2018): R945—R962. http://dx.doi.org/10.1152/ajpregu.00363.2017.

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The classical concepts of human sodium balance include 1) a total pool of Na+ of ≈4,200 mmol (total body sodium, TBS) distributed primarily in the extracellular fluid (ECV) and bone, 2) intake variations of 0.03 to ≈6 mmol·kg body mass−1·day−1, 3) asymptotic transitions between steady states with a halftime (T½) of 21 h, 4) changes in TBS driven by sodium intake measuring ≈1.3 day [ΔTBS/Δ(Na+ intake/day)], 5) adjustment of Na+ excretion to match any diet thus providing metabolic steady state, and 6) regulation of TBS via controlled excretion (90–95% renal) mediated by surrogate variables. The present focus areas include 1) uneven, nonosmotic distribution of increments in TBS primarily in “skin,” 2) long-term instability of TBS during constant Na+ intake, and 3) physiological regulation of renal Na+ excretion primarily by neurohumoral mechanisms dependent on ECV rather than arterial pressure. Under physiological conditions 1) the nonosmotic distribution of Na+ seems conceptually important, but quantitatively ill defined; 2) long-term variations in TBS represent significant deviations from steady state, but the importance is undetermined; and 3) the neurohumoral mechanisms of sodium homeostasis competing with pressure natriuresis are essential for systematic analysis of short-term and long-term regulation of TBS. Sodium homeostasis and blood pressure regulation are intimately related. Real progress is slow and will accelerate only through recognition of the present level of ignorance. Nonosmotic distribution of sodium, pressure natriuresis, and volume-mediated regulation of renal sodium excretion are essential intertwined concepts in need of clear definitions, conscious models, and future attention.

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Martin, Kylie, Sven-Jean Tan, and Nigel D. Toussaint. "Total Body Sodium Balance in Chronic Kidney Disease." International Journal of Nephrology 2021 (September 22, 2021): 1–10. http://dx.doi.org/10.1155/2021/7562357.

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Excess sodium intake is a leading but modifiable risk factor for mortality, with implications on hypertension, inflammation, cardiovascular disease, and chronic kidney disease (CKD). This review will focus mainly on the limitations of current measurement methods of sodium balance particularly in patients with CKD who have complex sodium physiology. The suboptimal accuracy of sodium intake and excretion measurement is seemingly more marked with the evolving understanding of tissue (skin and muscle) sodium. Tissue sodium represents an extrarenal influence on sodium homeostasis with demonstrated clinical associations of hypertension and inflammation. Measurement of tissue sodium has been largely unexplored in patients with CKD. Development and adoption of more comprehensive and dynamic assessment of body sodium balance is needed to better understand sodium physiology in the human body and explore therapeutic strategies to improve the clinical outcomes in the CKD population.

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Kitada, Kento, and Akira Nishiyama. "Revisiting blood pressure and body fluid status." Clinical Science 137, no. 9 (May 2023): 755–67. http://dx.doi.org/10.1042/cs20220500.

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Abstract Homeostasis of body fluid is a key component for maintaining health. An imbalance of body sodium and water causes various pathological states, such as dehydration, volume overload, hypertension, cardiovascular and renal diseases, and metabolic disorders. Conventional concepts regarding physiology and pathophysiology of body sodium and water balance have been established by several assumptions. These assumptions are that the kidneys are the master regulator of body sodium and water content, and that sodium moves inside the body in parallel with water. However, recent clinical and basic studies have proposed alternative concepts. These concepts are that body sodium and water balance are regulated by various organs and multiple factors, such as physical activity and the environment, and that sodium accumulates locally in tissues independently of the blood status and/or water. Various concerns remain unclear, and the regulatory mechanism of body sodium, fluid, and blood pressure needs to be readdressed. In the present review article, we discuss novel concepts regarding the regulation of body sodium, water, and blood pressure with a particular focus on the systemic water conservation system and fluid loss-triggered elevation in blood pressure.

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Titze, Jens, Natalia Rakova, Christoph Kopp, Anke Dahlmann, Jonathan Jantsch, and Friedrich C. Luft. "Balancing wobbles in the body sodium." Nephrology Dialysis Transplantation 31, no. 7 (September 25, 2015): 1078–81. http://dx.doi.org/10.1093/ndt/gfv343.

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Cross, W. G., and H. Ing. "Sodium Activation in the Human Body." Radiation Protection Dosimetry 10, no. 1-4 (January 1, 1985): 265–76. http://dx.doi.org/10.1093/rpd/10.1-4.265.

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Cross, W. G., and H. Ing. "Sodium Activation in the Human Body." Radiation Protection Dosimetry 10, no. 1-4 (January 1, 1985): 265–76. http://dx.doi.org/10.1093/oxfordjournals.rpd.a079428.

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10

Vieweg, W. V. R., and L. S. Godleski. "Psychosis, Body Weight and Plasma Sodium." British Journal of Psychiatry 153, no. 1 (July 1988): 122–23. http://dx.doi.org/10.1192/bjp.153.1.122b.

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Heer, Martina. "Sodium Regulation in the Human Body." Current Sports Medicine Reports 7, Suppl. 1 (July 2008): S3—S6. http://dx.doi.org/10.1249/jsr.0b013e31817f2241.

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12

Stefanidis, I., S. Stiller, V. Ikonomov, and H. Mann. "Sodium and body fluid homeostasis in profiling hemodialysis treatment." International Journal of Artificial Organs 25, no. 5 (May 2002): 421–28. http://dx.doi.org/10.1177/039139880202500512.

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Acute adverse side-effects of hemodialysis such as hypotension, muscle cramps, osmotic imbalance and thirst are induced by the interference with fluid and electrolyte balance occurring during treatment. Changes in osmolarity due to alterations of plasma sodium concentration during hemodialysis strongly influence fluid distribution between extracellular and intracellular fluid volume. Increased sodium dialysate concentration induces fluid shift from the intracellular to the extracellular compartment. This shift leads to a more efficient ultrafiltration by increasing plasma refilling volume but also to an increased thirst. Treatment of hypotension, cramps and nausea with hypertonic saline solution leads also to a considerable retention of sodium. Profiling hemodialysis consists in deliberately changing ultrafiltration and dialysate sodium in order to combine an efficient ultrafiltration with a balanced sodium handling and to prevent side-effects during treatment. Continuous measurement and control of blood volume seems to be the best method to prevent hypotensive episodes. Profiling of sodium should not be the cause of a positive sodium balance. The clinical benefits of sodium profiling to the patients have still to be proven.

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Palacios, Cristina, Karin Wigertz, and Connie M. Weaver. "Comparison of 24-Hour Whole Body versus Patch Tests for Estimating Body Surface Electrolyte Losses." International Journal of Sport Nutrition and Exercise Metabolism 13, no. 4 (December 2003): 479–88. http://dx.doi.org/10.1123/ijsnem.13.4.479.

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Purpose:To compare dermal electrolyte loss between whole body and regional patch methods in women during 24-h.Methods:Dermal loss was collected in 6 healthy women mean age 27 ± 4 years, while consuming 936 mg/d sodium, 1764 mg/d potassium, 696 mg/d calcium, and 152 mg/d magnesium. Twenty-four hour whole body dermal loss was collected using cotton suits by a washdown procedure. Twenty-four hour patch loss was collected from 8 patches placed on the legs, arms, and back.Results:Dermal loss from whole body was 108 ± 110 mg/d sodium, 133 ± 87 mg/d potassium, 103 ± 22 mg/d calcium, and 35 ± 13 mg/d magnesium. Electrolyte content from the 8 patches was similar among sites and ranged from 1.01–1.41 mg/d sodium, 0.35–0.83 mg/d potassium, 1.0– 1.45 mg/d calcium, and 0.43–0.49 mg/d magnesium. Projections from patches to whole body by the ratio of body surface area appear to overestimate actual whole body losses by 3.2X for sodium and calcium, 3.6X for magnesium, and 1.3X for potassium.Conclusions:Regional patch methods are more appropriate for relative comparisons than for accurately determining total daily dermal electrolyte losses.

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Kim, Ji-Hong. "Water and Sodium Balance of Body Fluid." Journal of the Korean Society of Pediatric Nephrology 14, no. 2 (2010): 111. http://dx.doi.org/10.3339/jkspn.2010.14.2.111.

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Munteanu, Constantin, and Alexandru Iliuta. "The role of sodium in the body." Balneo Research Journal 2, no. 2 (May 1, 2011): 70–74. http://dx.doi.org/10.12680/balneo.2011.1015.

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16

Staessen, Jan, Robert Fagard, Paul Lijnen, and Antoon Amery. "Body weight, sodium intake and blood pressure." Journal of Hypertension 7, Supplement 1 (February 1989): S19—S23. http://dx.doi.org/10.1097/00004872-198902001-00006.

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Whelton, Paul K. "Body Weight, Sodium, Potassium, and Blood Pressure." Journal of Clinical Hypertension 17, no. 12 (August 29, 2015): 926–28. http://dx.doi.org/10.1111/jch.12653.

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Trevisan, Maurizio, Pasquale Strazzullo, Franco Paulo Cappuccio, Eduardo Farinaro, Fabrizio Jossa, Vittorio Krogh, Roberto Iacone, and Mario Mancini. "Sodium-lithium countertransport and body fat distribution." Life Sciences 51, no. 9 (January 1992): 687–93. http://dx.doi.org/10.1016/0024-3205(92)90242-h.

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19

Bangerter, Neal K., Joshua D. Kaggie, Meredith D. Taylor, and J. Rock Hadley. "Sodium MRI radiofrequency coils for body imaging." NMR in Biomedicine 29, no. 2 (September 29, 2015): 107–18. http://dx.doi.org/10.1002/nbm.3392.

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20

Boicelli, C. A., and A. M. Giuliani. "Sodium ion distribution in the vitreous body." Magma: Magnetic Resonance Materials in Physics, Biology, and Medicine 4, no. 3-4 (September 1996): 241–45. http://dx.doi.org/10.1007/bf01772012.

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21

Frisbie, Malcolm Pratt, and William A. Dunson. "Seasonal aspects of sodium, potassium, and water balance in the predaceous diving beetle Dytiscus verticalis." Canadian Journal of Zoology 66, no. 7 (July 1, 1988): 1553–61. http://dx.doi.org/10.1139/z88-227.

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A previous study showed that food availability i the laboratory can dramatically affect sodium balance of the predaceous diving beetle Dytiscus verticalis. Because this species inhabits small ponds that dry up in the summer, it seemed likely that wild beetles would undergo annual changes in ody ion content. Seasonally collected predaceous diving beetles were analyzed for dry body mass, body water, body sodium and potassium, hemolymph sodium concentration, and hemolymph osmolality. Beetles varied in all characteristics over a 16-month period, and variation was seasonally cyclic for body water, body sodium, hemolymph sodium, and hemolymph osmolality, but not for dry mass and body potassium. A laboratory experiment and two field-enclosure experiments determined possible mechanisms underlying these cycles. Beetles in enclosures with food had greater dry mass than nonfed beetles in enclosures, but not greater than that of wild beetles. The number of tadpoles killed by beetles in enclosures correlated well with beetle dry mass. Because food availability directly affects dry mass, wild beetles must not suffer seasonal periods of food limitation. Body sodium and potassium levels also appear related to food availability, but not closely enough to explain the seasonal variation in sodium, the nonseasonal variation in potassium, and the nonparallel variation in the two cations. Food intake can be important for increasing both hemolymph sodium concentration and hemolymph osmolality, but these characteristics can be regulated independently of food intake and of each other. Seasonal variation in hemolymph sodium was out of phase with body sodium variation, suggesting that sodium supply is not the cause of hemolymph sodium cycles. Hemolymph osmolality was greatly increased in winter months, perhaps reflecting elevated levels of free amino acids in the hemolymph.

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22

Lopes‐Menezes, V. C., R. C. Dos‐Santos, V. Felintro, L. R. N. Monteiro, B. Paes‐Leme, D. Lustrino, E. A. Casartelli, L. Vivas, A. S. Mecawi, and L. C. Reis. "Acute body sodium depletion induces skin sodium mobilization in female Wistar rats." Experimental Physiology 104, no. 12 (October 24, 2019): 1754–61. http://dx.doi.org/10.1113/ep087998.

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23

Kapusta, D. R., and J. C. Obih. "Role of endogenous central opioid mechanisms in maintenance of body sodium balance." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 3 (March 1, 1995): R723—R730. http://dx.doi.org/10.1152/ajpregu.1995.268.3.r723.

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The role of endogenous central opioids in the regulation of renal function was studied in Sprague-Dawley rats. In metabolism studies, changes in sodium balance were examined during normal dietary sodium intake (days 1-7; Na+ of 174 meq/kg) and sodium restriction (days 8-14; Na+ of 4.0 meq/kg). The influence of endogenous central opioids was investigated by repeating the protocol in the same rats during intracerebroventricular infusion of the opioid antagonist naltrexone methylbromide (NMBR). Intracerebroventricular NMBR did not alter sodium balance in rats fed normal sodium chow. In contrast, on low-sodium days 8 and 9, rats exhibited a more negative sodium balance during intracerebroventricular NMBR (day 8; -1,191 +/- 37 mu eq) compared with respective predrug control levels (day 8; -641 +/- 39 mu eq). Subcutaneous NMBR did not alter renal adaptation to sodium restriction. Thus central opioids are not involved in the maintenance of sodium balance during normal sodium intake. However, when dietary sodium is restricted, central opioid pathways are activated as a mechanism to maximally retain sodium.

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Herlitz, Hans, Olof Jonsson, and Bengt-Åke Bengtsson. "Effect of Recombinant Human Growth Hormone on Cellular Sodium Metabolism." Clinical Science 86, no. 3 (March 1, 1994): 233–37. http://dx.doi.org/10.1042/cs0860233.

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1. The effect of treatment with recombinant human growth hormone on urinary sodium excretion, total body water, the renin-angiotensin system and erythrocyte sodium metabolism was investigated in 16 adults with growth hormone deficiency. 2. Total body water was determined by isotopic dilution, and erythrocyte electrolyte contents were analysed using flame photometry. The rate of sodium influx and the efflux rate constant of sodium were calculated from values of 22Na in erythrocytes in vitro. 3. One week of treatment with recombinant human growth hormone caused a decrease in urinary sodium excretion in 9/10 patients and an increase in erythrocyte sodium content. Total body water, plasma renin activity, angiotensin II concentration and transmembrane sodium transport were unaltered. 4. Six months of treatment with recombinant human growth hormone caused significant increases in total body water, erythrocyte sodium content and sodium transmembrane influx. Plasma renin activity tended to increase, whereas blood pressure and serum sodium and potassium concentrations remained unchanged. After 6 months on recombinant human growth hormone total body water showed a significant negative correlation with plasma renin activity. 5. The enhanced erythrocyte sodium transport, if this reflects what happens in the renal tubular cell, combined with a decrease in urinary sodium excretion, during treatment with recombinant human growth hormone could indicate an increase in tubular sodium reabsorption induced by the hormone. An increased plasma renin activity associated with the lack of blood pressure rise would reinforce sodium and water retention.

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Sun, Yijuan, David Mills, Todd S. Ing, Joseph I. Shapiro, and Antonios H. Tzamaloukas. "Body Sodium, Potassium and Water in Peritoneal Dialysis-Associated Hyponatremia." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 34, no. 3 (May 2014): 253–59. http://dx.doi.org/10.3747/pdi.2012.00201.

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Objective This report presents a method quantitatively analyzing abnormalities of body water and monovalent cations (sodium plus potassium) in patients on peritoneal dialysis (PD) with true hyponatremia. Methods It is well known that in the face of euglycemia serum sodium concentration is determined by the ratio between the sum of total body sodium plus total body potassium on the one hand and total body water on the other. We developed balance equations that enabled us to calculate excesses or deficits, relative to the state of eunatremia and dry weight, in terms of volumes of water and volumes of isotonic solutions of sodium plus potassium when patients presented with hyponatremia. We applied this method retrospectively to 5 episodes of PD-associated hyponatremia (serum sodium concentration 121–130 mEq/L) and compared the findings of the method with those of the clinical evaluation of these episodes. Results Estimates of the new method and findings of the clinical evaluation were in agreement in 4 of the 5 episodes, representing euvolemic hyponatremia (normal total body sodium plus potassium along with water excess) in 1 patient, hypovolemic hyponatremia (deficit of total body sodium plus potassium along with deficit of total body water) in 2 patients, and hypervolemic hyponatremia (excess of total body sodium along with larger excess of total body water) in 1 patient. In the 5th patient, in whom the new method suggested the presence of water excess and a relatively small deficit of monovalent cations, the clinical evaluation had failed to detect the cation deficit. Conclusions Evaluation of imbalances in body water and monovalent cations in PD-associated hyponatremia by the method presented in this report agrees with the clinical evaluation in most instances and could be used as a guide to the treatment of hyponatremia. Prospective studies are needed to test the potential clinical applications of this method.

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Siegler, Jason C., Amelia J. Carr, William T. Jardine, Lilia Convit, Rebecca Cross, Dale Chapman, Louise M. Burke, and Megan Ross. "The Hyperhydration Potential of Sodium Bicarbonate and Sodium Citrate." International Journal of Sport Nutrition and Exercise Metabolism 32, no. 2 (March 1, 2022): 74–81. http://dx.doi.org/10.1123/ijsnem.2021-0179.

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Buffering agents have not been comprehensively profiled in terms of their capacity to influence water retention prior to exercise. The purpose of this investigation was to profile the fluid retention characteristics of sodium bicarbonate (BIC) and sodium citrate (CIT) to determine the efficacy of these buffering mediums as hyperhydrating agents. Nineteen volunteers (13 males and six females; age = 28.3 ± 4.9 years) completed three trials (randomized and cross-over design). For each trial, a baseline measurement of body mass, capillary blood, and urine was collected prior to ingestion of their respective condition (control condition [CON] = 25 ml/kg artificially sweetened water; BIC condition = CON + 7.5 g/L of sodium in the form of BIC; CIT condition = CON + 7.5 g/L of sodium in the form of CIT). The fluid loads were consumed in four equal aliquots (0, 20, 40 and 60 min; fluid intake was 1.972 ± 361 ml [CON]; 1.977 ± 360 ml [BIC]; 1.953 ± 352 ml [CIT]). Samples were recorded at 20 (body mass and urine) and 60 min (blood) intervals for 180 min. Blood buffering capacity (HCO3−) was elevated (p < .001) in both BIC (32.1 ± 2.2 mmol/L) and CIT (28.9 ± 3.8 mmol/L) at 180 min compared with CON (25.1 ± 1.8 mmol/L). Plasma volume expansion was greater (p < .001) in both BIC (8.1 ± 1.3%) and CIT (5.9 ± 1.8%) compared with CON (−1.1 ± 1.4%); whereas, total urine production was lower in BIC and CIT at 180 min (BIC vs. CON, mean difference of 370 ± 85 ml; p < .001; CIT vs. CON, mean difference of 239 ± 102 ml; p = .05). There were no increases observed in body mass (p = .9). Under resting conditions, these data suggest BIC and CIT induce a greater plasma hypervolemic response as compared with water alone.

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Simpson, F. O., and Janet M. Ledingham. "Surfeit and Deficit of Sodium: Evidence from Studies of Body Sodium in Rats." Nephron 54, no. 1 (1990): 61–69. http://dx.doi.org/10.1159/000185811.

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Twigg, LE, RJ Mead, and DR King. "Metabolism of Fluoroacetate in the Skink (Tiliqua rugosa) and the Rat (Rattus norvegicus)." Australian Journal of Biological Sciences 39, no. 1 (1986): 1. http://dx.doi.org/10.1071/bi9860001.

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Administration of 100 mg sodium fiuoroacetate (compound 1080) per kilogram body weight to T. rugosa resulted in a 3 �4-fold increase in plasma citrate levels 48 h after dosing while administration of 3 mg sodium fiuoroacetate per kilogram body weight to R. norvegicus produced a fivefold increase in plasma citrate levels within 4 h. Administration of 300 mg sodium fiuoroacetate per kilogram body weight reduced the oxygen consumption of the skink by between 2�5 and 11 % while in the rat, 2 mg sodium fiuoroacetate per kilogram body weight reduced oxygen consumption by between 28 and 57%.

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Stumpf, Marcelo Tempel, Vivian Fischer, Giovani Jacob Kolling, Maira Balbinotti Zanela, Maria Edi Rocha Ribeiro, and Alexandre Süsenbach de Abreu. "Metabolic attributes, yield and stability of milk in Jersey cows fed diets containing sodium citrate and sodium bicarbonate." Pesquisa Agropecuária Brasileira 48, no. 5 (May 2013): 564–67. http://dx.doi.org/10.1590/s0100-204x2013000500014.

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The objective of this work was to evaluate the inclusion of sodium citrate and sodium bicarbonate in the diet of lactating Jersey cows, and its effects on the metabolic attributes, productivity and stability of milk. We evaluated urinary pH, levels of glucose and urea in blood, body weight, body condition score, milk yield, milk stability (ethanol test), and milk physicochemical properties of 17 cows fed diets containing sodium citrate (100 g per cow per day), sodium bicarbonate (40 g per cow per day) or no additives. Assessments were made at the 28th and 44th days. Supply of sodium citrate or bicarbonate has no influence on the metabolic attributes, productivity, body weight, and body condition score of the cows, neither on the composition and stability of milk.

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Mohamed, Ahmed, and Andrew Davenport. "Sodium loss, extracellular volume overload and hypertension in peritoneal dialysis patients treated by automated peritoneal dialysis cyclers." International Journal of Artificial Organs 43, no. 1 (August 12, 2019): 17–24. http://dx.doi.org/10.1177/0391398819864368.

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Introduction: Achieving sodium balance is important for peritoneal dialysis patients, as sodium excess may lead to hypertension and extracellular water expansion. We wished to determine whether greater sodium removal had adverse consequences. Methods: We calculated 24-h urinary and peritoneal sodium losses in peritoneal dialysis patients treated by automated cyclers, when attending for peritoneal membrane and bioimpedance assessments. Results: We reviewed 439 peritoneal dialysis patients, 56.7% male, average age 54.6 years, median sodium loss 110 (68–155) mmol/day. Sodium loss was strongly associated with urine volume, r = 0.37, protein nitrogen appearance rate, r = 0.29, and body cell mass, r = 0.21, all p < 0.001. We found no association with blood pressure or anti-hypertensive medication prescription, or extracellular water. On multivariable logistic regression analysis, sodium loss was associated with greater urine output, odds ratio 1.001, 95% confidence interval 1.00–1.001, p < 0.001, and protein nitrogen appearance (odds ratio 1.023, confidence interval 1.006–1.04), p = 0.008. Adjusting for body weight, sodium loss was associated with urine output (odds ratio 1.001, confidence interval 1.001–1.002, p < 0.001), and negatively with body fat index (odds ratio 0.96, confidence interval 0.93–0.99, p = 0.008) and co-morbidity grade (odds ratio 0.58, confidence interval 0.36–0.39, p = 0.023). Conclusion: Heavier peritoneal dialysis patients with greater estimated dietary protein intake (protein nitrogen appearance), those with greater residual renal function and peritoneal clearances, along with lower co-morbidity, had greater daily sodium losses. Adjusting for body weight, then sodium losses were greater with higher daily urine output, and lower in patients with proportionately more body fat and co-morbidity. Sodium losses would appear to primarily determined by body size and not associated with hypertension or extracellular water expansion.

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&NA;, &NA;. "Sodium, potassium, body mass, alcohol and blood pressure." Journal of Hypertension 6, no. 4 (December 1988): S584–586. http://dx.doi.org/10.1097/00004872-198812040-00183.

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Beretta-Piccoli, Carlo. "Body Sodium in Normal Subjects Predisposed to Hypertension." Journal of Cardiovascular Pharmacology 16 (1990): S52—S55. http://dx.doi.org/10.1097/00005344-199000167-00017.

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Beretta-Piccoli, Carlo. "Body Sodium in Normal Subjects Predisposed to Hypertension." Journal of Cardiovascular Pharmacology 16 (1990): S52—S55. http://dx.doi.org/10.1097/00005344-199006167-00017.

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Shinar, Hadassah, and Gil Navon. "Sodium-23 NMR relaxation times in body fluids." Magnetic Resonance in Medicine 3, no. 6 (December 1986): 927–34. http://dx.doi.org/10.1002/mrm.1910030613.

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Adrogué, Horacio J., Sreedhar Mandayam, Hocine Tighiouart, and Nicolaos E. Madias. "Osmotic and Nonosmotic Sodium Storage during Acute Hypertonic Sodium Loading." American Journal of Nephrology 50, no. 1 (2019): 11–18. http://dx.doi.org/10.1159/000501190.

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Background: The Edelman equation has long guided the expected response of plasma [Na+] to changes in sodium, potassium, and water balance, but recent short-term studies challenged its validity. Plasma [Na+] following hypertonic NaCl infusion in individuals on low-sodium diet fell short of the Edelman predictions supposedly because sodium restriction caused progressive osmotic inactivation of 50% of retained sodium. Here, we examine the validity of this challenge. Methods: We evaluated baseline total body water (TBW) and Na+ space following acute hypertonic NaHCO3 infusion in dogs with variable sodium and potassium stores, including normal stores, moderate depletion (chronic HCl feeding), or severe depletion (diuretics and dietary NaCl deprivation). Results: TBW (percentage body weight) averaged 65.9 in normals, 62.6 in HCl-induced metabolic acidosis and moderate sodium and potassium depletion, and 57.6 in diuretic-induced metabolic alkalosis and severe sodium and potassium depletion (p < 0.02). Na+ space (percentage body weight) at 30, 60, and 90 min postinfusion averaged 61.1, 59.8, and 56.1, respectively, in normals (p = 0.49); 70.0, 74.4, and 72.1, respectively, in acidotic animals (p = 0.21); and 56.4, 55.1, and 54.2, respectively, in alkalotic animals (p = 0.41). Absence of progressive expansion of Na+ space in each group disproves progressive osmotic inactivation of retained sodium. Na+ space at each time point was not significantly different from baseline TBW in normal and alkalotic animals indicating that retained sodium remained osmotically active in its entirety. However, Na+ space in acidotic animals at all times exceeded by ∼16% baseline TBW (p < 0.01) signifying an early, but nonprogressive, osmotic inactivation of retained sodium, which we link to baseline bone-sodium depletion incurred during acid buffering. Conclusions: Our investigation affirms the validity of the Edelman construct in normal dogs and dogs with variable sodium and potassium depletion and, consequently, refutes the recent observations in human volunteers subjected to dietary NaCl restriction.

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Laurén, Darrel Jon, and D. G. McDonald. "Acclimation to Copper by Rainbow Trout, Salmo gairdneri: Physiology." Canadian Journal of Fisheries and Aquatic Sciences 44, no. 1 (January 1, 1987): 99–104. http://dx.doi.org/10.1139/f87-012.

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Juvenile rainbow trout (Salmo gairdneri) were exposed to 55 μg copper∙L−1 for 28 d and then transferred to uncontaminated water for 7 d. Whole body sodium concentration and sodium uptake (Jin) were measured at weekly intervals; Jin was measured at various Na+ concentrations and kinetic parameters estimated. After 24 h of copper exposure, the maximum rate of sodium uptake (Jmax) was inhibited by 55%, the affinity for sodium (Km) reduced by 49%, and whole body Na+ decreased by about 12.5%. After 7 d of exposure, whole body Na+ had returned to control values, but Jmax was still inhibited by 41%. Recovery of whole body Na+ occurred largely by a reduction of sodium efflux (Jout). Both Jmax and Km continued to recover until day 28, at which time Jin had returned to control values. We conclude that acclimation to sublethal copper depends on changes in both Na+ transport and permeability.

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Takamata, A., G. W. Mack, C. M. Gillen, and E. R. Nadel. "Sodium appetite, thirst, and body fluid regulation in humans during rehydration without sodium replacement." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 266, no. 5 (May 1, 1994): R1493—R1502. http://dx.doi.org/10.1152/ajpregu.1994.266.5.r1493.

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After a 7-h H2O and Na+ depletion period (DP), produced by intermittent light exercise (8 bouts) at 35 degrees C, we examined thirst and taste palatability responses to 10 different NaCl solutions during 23 h of rehydration (RH) at 25 degrees C. During DP, net H2O and Na+ loss were 27.2 +/- 2.9 ml/kg and 3.29 +/- 0.45 meq/kg, respectively. Plasma osmolality (POsm) and plasma Na+ concentration ([Na+]p) increased significantly during DP by 3.4 +/- 1.2 mosmol/kgH2O and 3.0 +/- 1.0 meq/kgH2O, respectively. Plasma volume (PV) decreased by 6.5 +/- 1.9%. Thirst rating, renal fractional reabsorption of H2O, and plasma arginine vasopressin concentration (PAVP) increased as POsm increased. This increased thirst was accompanied by increased palatability ratings to H2O. During RH, subjects drank deionized H2O ad libitum and ate a Na(+)-free diet for 23 h. POsm and [Na+]p returned to control levels within 1 h RH and remained at or below the control thereafter. PV remained reduced by approximately 5% throughout RH. The increased thirst and PAVP returned to their respective control levels within 1 h of RH as POsm decreased, but thirst rating increased against between 17 and 23 h of RH without increase in POsm or PAVP. Palatability ratings to a 1 M NaCl solution at and after 3 h RH and palatability ratings to 0.3 M at 17 and 23 h RH were significantly higher than control. Plasma aldosterone concentration (PAldo) increased after DP, decreased with drinking, and increased again between 6 and 23 h of RH, accompanied by a marked decrease in fractional Na+ excretion to < 0.07%. Thus both Na+ preference and thirst in humans are influenced by body fluid and electrolyte status. The increased Na+ palatability (Na+ appetite) was preceded by osmotically induced thirst, and accompanied by nonosmotically driven thirst [extracellular fluid (ECF) thirst] and increased PAldo. The "Na+ appetite" and "ECF thirst" along with increased renal Na+ retention could contribute to ECF volume regulation after thermally induced H2O and Na+ depletion.

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Seeliger, Erdmann, Katrin Lohmann, Benno Nafz, Pontus B. Persson, and H. Wolfgang Reinhardt. "Pressure-dependent renin release: effects of sodium intake and changes of total body sodium." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 2 (August 1, 1999): R548—R555. http://dx.doi.org/10.1152/ajpregu.1999.277.2.r548.

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The impact of sodium intake and changes in total body sodium (TBS) for the setting of pressure-dependent renin release (PDRR) was studied in freely moving dogs. An aortic cuff allowed servo control of renal perfusion pressure (RPP) at preset values. Protocols were 1) high sodium intake (HSI), 2) low sodium intake (LSI), 3) TBS moderately increased (+3.1 mmol Na/kg body wt) by 20% reduction of RPP for 2–4 days, 4) large increase of TBS (+8.2) by combining protocol 3 with aldosterone infusion, and 5) TBS reduced (−3.1) by peritoneal dialyses. Twenty-four-hour time courses of arterial plasma renin activity (PRA) revealed that LSI increased PRA for the first 10 h only; afterward PRA did not differ between LSI and HSI. Reduced TBS increased PRA constantly, and the large increase of TBS constantly reduced PRA. PDRR stimulus-response curves (assessed 20 h after last sodium intake) revealed an exponential relationship in each protocol. PDRR was not changed by different sodium intake. Conversely, reduced TBS increased PDRR markedly, whereas the large increase of TBS suppressed it. Thus an inverse relationship between TBS and PRA, i.e., a TBS-dependent renin release, was found. This relationship was enhanced by decreasing RPP. This interplay between TBS-dependent renin release and PDRR allows the organism a differentiated reaction to changes in TBS and arterial pressure.

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Segar, Jeffrey L., Connie C. Grobe, and Justin L. Grobe. "Fetal storage of osmotically inactive sodium." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 318, no. 3 (March 1, 2020): R512—R514. http://dx.doi.org/10.1152/ajpregu.00336.2019.

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Work in adult humans and animals suggest sodium (Na) is stored in tissue reservoirs without commensurate water retention. These stores may protect from water loss, regulate immune function, and participate in blood pressure regulation. A role for such stores early in life, during which total body Na sufficiency is vital for optimal growth, has not been explored. Using data from previously published literature, we calculated total body stores of Na, potassium (K), and chloride (Cl) during fetal development (24–40 wk gestation) using two methods 1) based on the distribution of body water mass within extracellular and intracellular compartments, and 2) reported total mineral content. Based on differences between the models, we argue that Na, and to a lesser extent Cl, but not K, are stored in osmotically inactive pools within the fetus that increase with advancing gestational age. Because human breastmilk is relatively Na deficient, we speculate the fetal osmotically inactive Na pool is vital for providing a sufficient total body Na content that supports optimal postnatal growth.

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Marlita, Jeli, Yuyun Febriani, Risma Hayatun Nufus, Muhlisun Azim, and Baiq Maylinda Gemantari. "ANALYSIS OF NaOCl CONTENT OF HAND & BODY LOTION AND FACE WASH CREAM BY IODOMETRIC TITRATION METHOD." Medical Sains : Jurnal Ilmiah Kefarmasian 9, no. 2 (June 6, 2024): 417–22. http://dx.doi.org/10.37874/ms.v9i2.1242.

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Cosmetics are needed by the public, such as hand and body lotions and face brightening creams, and there are many misuses of hazardous chemicals in cosmetics, including lotions and face brightening creams. Sodium hypochlorite, a hazardous chemical, can cause skin damage, such as irritation, rash, hypersensitivity, and burns. The purpose of this study was to determine the presence of sodium hypochlorite compounds and sodium hypochlorite in hand and body lotion cosmetics and face brightening cream. The method used in this research was qualitative analysis with color reaction and quantitative analysis with iodometric titration. The results qualitatively showed that color changes occurred in all samples. NaOCl concentration in hand and body lotion at 0.2% concentration showed an average NaOCl concentration of 3.263 % ± 0.25 and face brightening cream concentration at an average concentration of 10 mg showed NaOCl levels of 88.933 % ± 7.57. Based on this, it was concluded that in the samples of hand and body lotion and face brightening cream, sodium hypochlorite compounds with different levels. Therefore, these samples could have side effects and toxicity in their usefulness as cosmetics. Keywords: Hand & body lotion, face brightening cream, sodium hypochlorite (NaOCl), iodometric titration

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Tremblay, Angelo, Marie-Pascale Gagné, Louis Pérusse, Catherine Fortier, Véronique Provencher, Ronan Corcuff, Sonia Pomerleau, Nicoletta Foti, and Vicky Drapeau. "Sodium and Human Health: What Can Be Done to Improve Sodium Balance beyond Food Processing?" Nutrients 16, no. 8 (April 18, 2024): 1199. http://dx.doi.org/10.3390/nu16081199.

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Sodium plays a key role in the regulation of water balance and is also important in food formulation due to its contribution to the taste and use in the preservation of many foods. Excessive intake of any essential nutrient is problematic and this seems to be particularly the case for sodium since a high intake makes it the nutrient most strongly associated with mortality. Sodium intake has been the object of recommendations by public health agencies such as the WHO and this has resulted in efforts by the food industry to reduce the sodium content of packaged foods, although there is still room for improvement. The recent literature also emphasizes the need for other strategies, e.g., regulations and education, to promote adequate sodium intake. In the present paper, we also describe the potential benefits of a global healthy lifestyle that considers healthy eating but also physical activity habits that improve body functionality and may help to attenuate the detrimental effects of high sodium intake on body composition and cardiometabolic health. In conclusion, a reduction in sodium intake, an improvement in body functioning, and educational interventions promoting healthy eating behaviours seem to be essential for the optimal regulation of sodium balance.

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Reinhardt, H. Wolfgang, and Erdmann Seeliger. "Toward an Integrative Concept of Control of Total Body Sodium." Physiology 15, no. 6 (December 2000): 319–25. http://dx.doi.org/10.1152/physiologyonline.2000.15.6.319.

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Total body sodium (TBSodium) is a major determinant of body water and arterial pressure. Several observations, in particular that of a “sodium memory,” indicate that TBSodium is a controlled variable. Various regulatory elements are involved, e.g., the renin-angiotensin-aldosterone system, atrial receptors, and renal arterial pressure. Balance studies in dogs provide new insights into their contributions to TBSodium control.

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White, B. D., G. L. Edwards, and R. J. Martin. "Interaction of type I and type II corticosteroid receptor stimulation on carcass energy and carcass water." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, no. 5 (May 1, 1996): R1099—R1108. http://dx.doi.org/10.1152/ajpregu.1996.270.5.r1099.

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The effects of chronic type I and type II corticosteroid receptor stimulation were examined in adrenalectomized Sprague-Dawley rats to quantify the relative contribution of body energy and body water changes to changes in body weight. Adrenalectomy caused a decrease in both body energy and water. Aldosterone (type I agonist) treatment increased body weight gain and returned energy accretion to the level of sham-operated animals. However, most of the change in body weight (72%) was attributable to a change in body water. The aldosterone-induced increase in body weight gain and carcass water were attenuated by RU-28362 (type II receptor agonist) infusion, suggesting that type II receptor stimulation can antagonize the effect of type I receptor stimulation. Changes in carcass water were paralleled by changes in soluble carcass sodium. Despite alterations in soluble body sodium, no measurable differences in cumulative sodium retention were found. These findings confirm previous studies suggesting an effect of type I receptor stimulation on energy accretion. However, they also caution that changes in body weight cannot be equated with changes in body energy.

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Yanwittayakul, Krittin, Tararat Khaokhiew, Woraphan Chaisriratanakul, Win Bunjongpru, and Sira Srinives. "Fabrication of an ISFET Sensor for the Detection of Sodium Ions in Body Plasma." Key Engineering Materials 824 (October 2019): 190–96. http://dx.doi.org/10.4028/www.scientific.net/kem.824.190.

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Sodium chloride, commonly known as table salt, is widely used as essential seasoning in food, snacks and deserts worldwide. However, excessive consumption of table salt is a major cause of various health issues, involving high blood pressure, liver cirrhosis, kidney disease, and heart failure. This research aims at creating a portable, low-powered, efficient sensor for detection of sodium ions in body plasma for medical diagnosis purpose. The device was fabricated on a platform of Ion-Sensitive Field-Effect Transistor (ISFET) modified with sodium ionophore (sodium recognizing element), entrapped in polyurethane thin film. Our preliminary studies show that sodium ionophore-modified ISFET sensor yields good sensing performances, having a maximum sensitivity of 43 mV/pNa, and a detection limit of 2.3 millimol/liter.

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Sokolař, Radomír, and Lucie Vodová. "Sodium Hexametaphosphate as Deflocculation Agent for Calcium Aluminate Cements in Porcelain Body." Advanced Materials Research 897 (February 2014): 30–33. http://dx.doi.org/10.4028/www.scientific.net/amr.897.30.

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Influence of typical ceramic deflocculant – sodium hexametaphosphate – on the rheological properties (viscosity) of calcium aluminate cement paste, porcelain raw materials mixture (casting slip), and fired porcelain body respectively, was determined. It was used two different typed of calcium aluminate cements (from two sources – producers - Istra, Almatis) with different content of Al2O3 (40 % and 70 %). Sodium hexametaphosphate decreases of water content needed to prepare slip casting with constant viscosity. Deflocculant increases the modulus of rupture MOR of dried green body and its bulk density. Sodium hexametaphosphate admixture is very suitable for the creation of porcelain body with low porosity after firing.

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46

Simpson, F. O. "The Control of Body Sodium in Relation to Hypertension." Journal of Cardiovascular Pharmacology 16 (1990): S27—S30. http://dx.doi.org/10.1097/00005344-199000167-00010.

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Simpson, F. O. "The Control of Body Sodium in Relation to Hypertension." Journal of Cardiovascular Pharmacology 16 (1990): S27—S30. http://dx.doi.org/10.1097/00005344-199006167-00010.

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Alderman, M. H., H. W. Cohen, and J. Fang. "DIET SODIUM, BODY MASS INDEX, EXERCISE AND CARDIOVASCULAR EVENTS." Journal of Hypertension 22, Suppl. 1 (February 2004): S5. http://dx.doi.org/10.1097/00004872-200402001-00005.

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Geraci, J. P., K. L. Jackson, and M. S. Mariano. "Fluid and Sodium Loss in Whole-Body-Irradiated Rats." Radiation Research 111, no. 3 (September 1987): 518. http://dx.doi.org/10.2307/3576937.

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Baker, Lindsay B., Ryan P. Nuccio, Adam J. Reimel, Shyretha Brown, Corey T. Ungaro, Peter JD De Chavez, and Kelly A. Barnes. "Cross-validation Of Whole Body Sweat Sodium Prediction Equations." Medicine & Science in Sports & Exercise 52, no. 7S (July 2020): 969. http://dx.doi.org/10.1249/01.mss.0000686096.35530.dc.

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Journal articles on the topic 'Sodium in the body'

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