Dietary Sodium Intake: A Determinant of Postprandial Plasma Sodium Concentration in the Dog

1982 ◽  
Vol 62 (5) ◽  
pp. 471-477 ◽  
Author(s):  
E. G. Schneider ◽  
Sarah D. Gleason ◽  
A. Zucker
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Free Access ◽  
Potassium Excretion ◽  
Plasma Sodium Concentration

1. The effect of dietary sodium intake on pre-and post-prandial plasma sodium concentrations and on the pattern of sodium and potassium excretion was determined in conscious female dogs, who were allowed free access to water and were fed on commercial low sodium diets supplemented with 0, 50, 100 or 250 mmol of sodium chloride/day for 6 days. 2. The preprandial plasma sodium concentration was not altered by the dietary sodium intake. However, the 4 h postprandial plasma sodium concentration was linearly related to the magnitude of dietary sodium intake, whereas the 8 h postprandial plasma sodium concentration was elevated only in dogs receiving 250 mmol of sodium/day. 3. The (0–8 h/0–24 h) ratio for urinary sodium excretion was significantly correlated with both the dietary sodium intake and the postprandial increase in plasma sodium concentration. 4. The 24 h excretion of potassium was not markedly affected by the dietary sodium intake; however, the (0–8 h/0–24 h) ratio for potassium excretion was significantly correlated with both the dietary sodium intake and the (0–8 h/0–24 h) ratio for sodium excretion. 5. These data indicate that: (a) postprandial increases in plasma sodium concentration need to be considered when evaluating the mechanisms involved in the daily regulation of sodium balance; (b) the daily pattern of potassium excretion is closely linked to the dietary sodium intake.

Effect of Hypertonic and Hypotonic Infusions on Aldosterone in Conscious Sodium-Depleted Dogs

1981 ◽  
Vol 61 (2) ◽  
pp. 191-199 ◽  
Author(s):  
Jennifer W. Childers ◽  
E. G. Schneider
Keyword(s):  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Plasma Aldosterone ◽  
Plasma Sodium ◽  
Aldosterone Secretion ◽  
Plasma Aldosterone Concentration ◽  
Plasma Sodium Concentration ◽  
Sodium Load

1. The role of the plasma sodium concentration in the regulation of aldosterone secretion and sodium excretion was investigated by comparing in 13 conscious sodium-depleted dogs the effects of the same sodium load (2.5 mmol/kg) given as either a hypertonic or hypotonic infusion. 2. The plasma sodium concentration was significantly higher and the plasma aldosterone concentration and urinary aldosterone excretion were significantly lower after the hypertonic infusion as compared with the hypotonic infusion. 3. The cumulative urinary sodium excretion during the 22 h after beginning the infusion was significantly greater after the hypertonic infusion, but this difference was not observed in five sodium-depleted dogs who were treated with deoxycorticosterone acetate before the infusions were given. 4. These data suggest that elevations in plasma sodium concentration are effective in decreasing aldosterone secretion and, hence, in increasing sodium excretion in conscious sodium-depleted dogs.

scholarly journals Association between 24-h urinary sodium and potassium excretion and blood pressure among Chinese adults aged 18–69 years

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiaofu Du ◽  
Le Fang ◽  
Jianwei Xu ◽  
Xiangyu Chen ◽  
Yamin Bai ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Inverse Association ◽  
Potassium Excretion ◽  
Chinese Adults ◽  
Potassium Intake ◽  
Sodium And Potassium

AbstractThe direction and magnitude of the association between sodium and potassium excretion and blood pressure (BP) may differ depending on the characteristics of the study participant or the intake assessment method. Our objective was to assess the relationship between BP, hypertension and 24-h urinary sodium and potassium excretion among Chinese adults. A total of 1424 provincially representative Chinese residents aged 18 to 69 years participated in a cross-sectional survey in 2017 that included demographic data, physical measurements and 24-h urine collection. In this study, the average 24-h urinary sodium and potassium excretion and sodium-to-potassium ratio were 3811.4 mg/day, 1449.3 mg/day, and 4.9, respectively. After multivariable adjustment, each 1000 mg difference in 24-h urinary sodium excretion was significantly associated with systolic BP (0.64 mm Hg; 95% confidence interval [CI] 0.05–1.24) and diastolic BP (0.45 mm Hg; 95% CI 0.08–0.81), and each 1000 mg difference in 24-h urinary potassium excretion was inversely associated with systolic BP (− 3.07 mm Hg; 95% CI − 4.57 to − 1.57) and diastolic BP (− 0.94 mm Hg; 95% CI − 1.87 to − 0.02). The sodium-to-potassium ratio was significantly associated with systolic BP (0.78 mm Hg; 95% CI 0.42–1.13) and diastolic BP (0.31 mm Hg; 95% CI 0.10–0.53) per 1-unit increase. These associations were mainly driven by the hypertensive group. Those with a sodium intake above about 4900 mg/24 h or with a potassium intake below about 1000 mg/24 h had a higher risk of hypertension. At higher but not lower levels of 24-h urinary sodium excretion, potassium can better blunt the sodium-BP relationship. The adjusted odds ratios (ORs) of hypertension in the highest quartile compared with the lowest quartile of excretion were 0.54 (95% CI 0.35–0.84) for potassium and 1.71 (95% CI 1.16–2.51) for the sodium-to-potassium ratio, while the corresponding OR for sodium was not significant (OR, 1.28; 95% CI 0.83–1.98). Our results showed that the sodium intake was significantly associated with BP among hypertensive patients and the inverse association between potassium intake and BP was stronger and involved a larger fraction of the population, especially those with a potassium intake below 1000 mg/24 h should probably increase their potassium intake.

scholarly journals Spot urine and 24-h diet recall estimates of dietary sodium intake from the 2008/09 New Zealand Adult Nutrition Survey: a comparison

2020 ◽  
Author(s):  
RM McLean ◽  
SM Williams ◽  
Lisa Te Morenga ◽  
JI Mann
Keyword(s):  
New Zealand ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Dietary Sodium ◽  
Urine Collection ◽  
Limits Of Agreement ◽  
Nutrition Survey ◽  
Spot Urine ◽  
Diet Recall

© 2018, Macmillan Publishers Limited, part of Springer Nature. Background: We aimed to test the difference between estimates of dietary sodium intake using 24-h diet recall and spot urine collection in a large sample of New Zealand adults. Methods: We analysed spot urine results, 24-h diet recall, dietary habits questionnaire and anthropometry from a representative sample of 3312 adults aged 15 years and older who participated in the 2008/09 New Zealand Adult Nutrition Survey. Estimates of adult population sodium intake were derived from 24-h diet recall and spot urine sodium using a formula derived from analysis of INTERSALT data. Correlations, limits of agreement and mean difference were calculated for the total sample, and for population subgroups. Results: Estimated total population 24-h urinary sodium excretion (mean (95% CI)) from spot urine samples was 3035 mg (2990, 3079); 3612 mg (3549, 3674) for men and 2507 mg (2466, 2548) for women. Estimated mean usual daily sodium intake from 24-h diet recall data (excluding salt added at the table) was 2564 mg (2519, 2608); 2849 mg (2779, 2920) for men and 2304 mg (2258, 2350) for women. Correlations between estimates were poor, especially for men, and limits of agreement using Bland–Altman mean difference analysis were wide. Conclusions: There is a poor agreement between estimates of individual sodium intake from spot urine collection and those from 24-hour diet recall. Although, both 24-hour dietary recall and estimated urinary excretion based on spot urine indicate mean population sodium intake is greater than 2 g, significant differences in mean intake by method deserve further investigation in relation to the gold standard, 24-hour urinary sodium excretion.

scholarly journals 24-Hour vs. Spot Urinary Sodium and Potassium Measurements in Adult Hypertensive Patients: A Cohort Validation Study

2019 ◽  
Vol 32 (10) ◽  
pp. 983-991
Author(s):  
Elizabeth R Wan ◽  
Jennifer Cross ◽  
Reecha Sofat ◽  
Stephen B Walsh
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Serum Biochemistry ◽  
Urinary Sodium ◽  
Hypertensive Patients ◽  
Spot Urine ◽  
Sodium Ingestion ◽  
Weak Negative Correlation

Abstract BACKGROUND Sodium intake is correlated with the development of hypertension. Guyton’s principals suggest that the 24-hour urinary sodium excretion reflects sodium ingestion over the same period. 24-hour urine collections are arduous to collect, so many centers use spot urinary measurements instead. We compared spot to matched 24-hour urinary electrolyte measurements. METHODS We examined 419 hypertensive patients from the UCL Complex Hypertension Clinic. 77 had matched and complete 24-hour and spot urinary and serum biochemistry to examine. We compared the spot and 24-hour urinary; sodium concentration, Na/Cr ratio, FENa, Kawasaki and Tanaka estimated sodium excretion as well as the potassium concentration, K/Cr ratio, Kawasaki and Tanaka potassium excretion. RESULTS Our cohort was 58% male and the median age was 41 years. The 24-hour and spot Na concentrations correlated moderately (r = 0.4633, P < 0.0001). The 24-hour and spot Na/creatinine ratios correlated weakly (r = 0.2625, P = 0.0194). The 24-hour and spot FENa results showed a weak negative correlation (r = −0.222, P = ns). The 24-hour sodium excretion and the Kawasaki-derived spot urine sodium excretion correlated moderately (r = 0.3118, P = 0.0052). All Bland–Altman analyses showed poor agreement. The 24-hour and spot potassium concentrations correlated very poorly (r = 0.1158, P = ns). The 24-hour and spot urinary K/creatinine ratios correlated weakly (r = 0.47, P ≤ 0.0001). 24-hour and Kawasaki and Tanaka estimated potassium excretions correlated much better (r = 0.58, P < 0.0001). CONCLUSIONS Spot urinary measurements of sodium give a very poor understanding of the natriuresis occurring over the same 24-hour period. The Kawasaki and Tanaka estimations of the 24-hour sodium excretion showed a much lower correlation than previously reported.

Sodium Excretion in Man, and Adaptation to a Low-Sodium Diet: Effect of Intravenous Sodium Chloride

1979 ◽  
Vol 57 (3) ◽  
pp. 225-231 ◽  
Author(s):  
D. Gordon ◽  
W. S. Peart
Keyword(s):  
Sodium Chloride ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Plasma Sodium ◽  
Normal Male ◽  
Renal Sodium Excretion ◽  
Portal Monitor ◽  
Intravenous Sodium ◽  
Oral Sodium

1. The aim of this study was to test whether a postulated gastrointestinal or portal monitor of sodium intake plays any part in adjusting renal sodium excretion when dietary sodium is reduced. 2. Normal male subjects were given 50 mmol of sodium chloride intravenously three times daily for 3 days to replace or to supplement a constant oral intake of sodium chloride. 3. When oral sodium chloride was replaced with intravenous sodium chloride, renal sodium excretion remained constant. 4. When oral sodium chloride was kept constant, sodium administered as intravenous sodium chloride was promptly excreted in three out of four subjects. There was a delay in the increase in sodium excretion in the fourth subject. 5. Infusions containing 50 mmol of sodium chloride in 50 ml given intravenously over 22 min produced a rise in plasma sodium concentration and a fall in concentration of total plasma solids. 6. These results provide no evidence for a gastrointestinal or portal monitor of sodium intake, but do not disprove the existence of such a monitor.

The Antidiuretic Effect of Chronic Hydrochlorothiazide Treatment in Rats with Diabetes Insipidus: Water and Electrolyte Balance

1982 ◽  
Vol 63 (6) ◽  
pp. 525-532 ◽  
Author(s):  
S. J. Walter ◽  
J. Skinner ◽  
J. F. Laycock ◽  
D. G. Shirley
Keyword(s):  
Diabetes Insipidus ◽  
Extracellular Volume ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Electrolyte Balance ◽  
Antidiuretic Effect

1. The antidiuretic effect of hydrochlorothiazide in diabetes insipidus was investigated in rats with the hereditary hypothalamic form of the disease (Brattleboro rats). 2. Administration of hydrochlorothiazide in the food resulted in a marked fall in urine volume and a corresponding rise in osmolality. These effects persisted throughout the period of treatment (6–7 days). 3. Body weight and extracellular volume were significantly reduced in the thiazide-treated rats. 4. Hydrochlorothiazide caused an increase in urinary sodium excretion only on the first day of treatment. The resulting small negative sodium balance (in comparison with untreated rats) remained statistically significant for 2 days only. Thiazide-treated rats gradually developed a potassium deficit which was statistically significant from the fourth day of treatment. 5. Total exchangeable sodium, measured after 7 days of thiazide treatment, was not significantly different from that of untreated rats. However, plasma sodium was reduced in thiazide-treated animals, whereas erythrocyte sodium concentration was elevated. 6. It is concluded that the antidiuresis resulting from chronic hydrochlorothiazide administration is associated with a reduction in extracellular volume, but not with a significant overall sodium deficit. Hydrochlorothiazide appears to cause a redistribution of the body's sodium such that the amount of sodium in the extracellular fluid compartment is reduced.

scholarly journals Spot urine and 24-h diet recall estimates of dietary sodium intake from the 2008/09 New Zealand Adult Nutrition Survey: a comparison

2020 ◽  
Author(s):  
RM McLean ◽  
SM Williams ◽  
Lisa Te Morenga ◽  
JI Mann
Keyword(s):  
New Zealand ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Dietary Sodium ◽  
Urine Collection ◽  
Limits Of Agreement ◽  
Nutrition Survey ◽  
Spot Urine ◽  
Diet Recall

© 2018, Macmillan Publishers Limited, part of Springer Nature. Background: We aimed to test the difference between estimates of dietary sodium intake using 24-h diet recall and spot urine collection in a large sample of New Zealand adults. Methods: We analysed spot urine results, 24-h diet recall, dietary habits questionnaire and anthropometry from a representative sample of 3312 adults aged 15 years and older who participated in the 2008/09 New Zealand Adult Nutrition Survey. Estimates of adult population sodium intake were derived from 24-h diet recall and spot urine sodium using a formula derived from analysis of INTERSALT data. Correlations, limits of agreement and mean difference were calculated for the total sample, and for population subgroups. Results: Estimated total population 24-h urinary sodium excretion (mean (95% CI)) from spot urine samples was 3035 mg (2990, 3079); 3612 mg (3549, 3674) for men and 2507 mg (2466, 2548) for women. Estimated mean usual daily sodium intake from 24-h diet recall data (excluding salt added at the table) was 2564 mg (2519, 2608); 2849 mg (2779, 2920) for men and 2304 mg (2258, 2350) for women. Correlations between estimates were poor, especially for men, and limits of agreement using Bland–Altman mean difference analysis were wide. Conclusions: There is a poor agreement between estimates of individual sodium intake from spot urine collection and those from 24-hour diet recall. Although, both 24-hour dietary recall and estimated urinary excretion based on spot urine indicate mean population sodium intake is greater than 2 g, significant differences in mean intake by method deserve further investigation in relation to the gold standard, 24-hour urinary sodium excretion.

Chronic sodium loading augments natriuretic response to acute volume expansion in the preweaned rat

1995 ◽  
Vol 269 (1) ◽  
pp. R15-R22 ◽  
Author(s):  
D. G. Muchant ◽  
B. A. Thornhill ◽  
D. C. Belmonte ◽  
R. A. Felder ◽  
A. Baertschi ◽  
...  
Keyword(s):  
Volume Expansion ◽  
Sodium Intake ◽  
Somatic Growth ◽  
Sodium Concentration ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Urinary Flow ◽  
Adult Rats ◽  
High Sodium ◽  
Before And After

Positive sodium balance is necessary for normal somatic growth of the neonate, and the neonatal renal response to volume expansion (VE) is attenuated compared with the adult. To test the hypothesis that dietary sodium modulates the developmental response to VE, preweaned rats were artificially reared with either a normal (25 meq/l)- or high-sodium (145 meq/l) diet for 7-8 days and were compared with adult rats receiving normal or high sodium. Serum sodium concentration remained normal in adults on high sodium, whereas neonates became hypernatremic. Glomerular filtration rate (GFR), urinary flow (V), and urinary sodium (UNaV) were measured before and after acute saline VE (1% body wt). While remaining constant in preweaned rats, GFR increased > 50% in adult rats after VE (P < 0.05). High sodium intake augmented V and UNaV after VE but was not sustained in neonates as in adults. Plasma atrial natriuretic peptide (ANP) and guanosine 3',5'-cyclic monophosphate excretion (UcGMPV) were measured, and baseline UcGMPV was lower in preweaned rats receiving normal sodium but increased to levels similar to adult levels after VE. Postexpansion plasma ANP was higher in preweaned rats than in adult rats and was not affected by dietary sodium regardless of age. We conclude that the attenuated postexpansion natriuresis in the neonate is due in part to an adaptive response to limited sodium intake. However, neonatal compensation to increased sodium intake is incomplete and independent of plasma ANP.

scholarly journals Elevated cerebrospinal fluid sodium in hypertensive human subjects with a family history of Alzheimer’s disease

2020 ◽  
Vol 52 (3) ◽  
pp. 133-142
Author(s):  
Lucas A. C. Souza ◽  
Fatima Trebak ◽  
Veena Kumar ◽  
Ryousuke Satou ◽  
Patrick G. Kehoe ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Sodium Intake ◽  
Human Subjects ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Chronic Hypertension ◽  
Plasma Sodium Concentration ◽  
History Of

High salt (sodium) intake leads to the development of hypertension despite the fact that plasma sodium concentration ([Na+]) is usually normal in hypertensive human patients. Increased cerebrospinal fluid (CSF) sodium contributes to elevated sympathetic activity and high blood pressure (BP) in rodent models of hypertension. However, whether there is an increased accumulation of sodium in the CSF of humans with chronic hypertension is not well defined. Here, we investigated CSF [Na+] from hypertensive and normotensive human subjects with family histories of Alzheimer’s disease in samples collected in a clinical trial, as spinal tap is not a routine clinical procedure for hypertensive patients. The [Na+] and osmolality in plasma and CSF were measured by flame photometry. Daytime ambulatory BP was monitored while individuals were awake. Participants were deidentified and data were analyzed in conjunction with a retrospective analysis of patient history and diagnosis. We found that CSF [Na+] was significantly higher in participants with high BP compared with normotensive participants; there was no difference in plasma [Na+], or plasma and CSF osmolality between groups. Subsequent multiple linear regression analyses controlling for age, sex, race, and body mass index revealed a significant positive correlation between CSF [Na+] and BP but showed no correlation between plasma [Na+] and BP. In sum, CSF [Na+] was higher in chronic hypertensive individuals and may play a key role in the pathogenesis of human hypertension. Collectively, our findings provide evidence for the clinical significance of CSF [Na+] in chronic hypertension in humans.

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