The Effect of Brain Extracts on Urinary Sodium Excretion of the Rat and the Intracellular Sodium Concentration of Renal Tubule Fragments

1974 ◽  
Vol 47 (3) ◽  
pp. 201-213 ◽  
Author(s):  
E. M. Clarkson ◽  
K. G. Koutsaimanis ◽  
M. Davidman ◽  
M. Du Bois ◽  
W. P. Penn ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Gel Filtration ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Significant Rise ◽  
Intracellular Sodium ◽  
Urinary Sodium ◽  
Conscious Rat ◽  
Intracellular Sodium Concentration ◽  
Brain Extracts

1. Extracts were prepared from bovine hypothalamus and cerebral cortex by gel filtration on Sephadex G-25 and G-50. 2. The vasopressin in the hypothalamic extracts was inactivated with thioglycollate and the effectiveness of inactivation was tested in the alcohol-anaesthetized rat. 3. The inactivated hypothalamic extracts caused a significant rise, and the cortical extracts an insignificant fall, in the urinary sodium excretion of the conscious rat. 4. Incubation of tubule fragments in hypothalamic extracts caused a significant rise in intracellular sodium concentration of the tubules when compared with incubation in Ringer, whereas incubation in cortical extracts caused a rise which was not significant. Nevertheless the rise in intracellular sodium concentration produced by incubating the tubules in hypothalamic extracts was not significantly different from the rise produced by incubation in cortical extracts.

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.

Further Evidence in Vivo for a Circulating Natriuretic Substance after Expanding the Blood Volume in Rats

1980 ◽  
Vol 59 (6) ◽  
pp. 423-433 ◽  
Author(s):  
Catherine A. Knock
Keyword(s):  
Blood Volume ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Significant Rise ◽  
Urinary Sodium ◽  
Bilateral Nephrectomy ◽  
Experimental Protocol ◽  
Equivalent Time

1. The blood volume of 18 rats was expanded with blood with which they were equilibrated. In another 18 rats undergoing the same experimental protocol, the blood volume was not expanded. 2. In some rats the urine was reinfused. 3. A 1 ml portion of plasma obtained either 1 h after the blood volume was expanded, or at an equivalent time from the control rats, was injected intravenously into an assay rat. 4. The injection of plasma produced a gradual and significant rise in sodium excretion in the assay rat when it was obtained from an animal with an expanded blood volume, the urine of which was being reinfused. 5. When the increase in blood volume was sustained by a preceding bilateral nephrectomy, instead of urine reinfusion, the injection of 1 ml of plasma into an assay rat did not cause a rise in urinary sodium excretion. 6. It is concluded that the natriuresis involved in the assay rat was caused by a natriuretic substance in the 1 ml of plasma obtained from the blood-volume-expanded urine-reinfused rat. 7. The experiments suggest that the natriuretic substance is excreted in the urine and may be produced in the kidney.

EFFECTS OF 9-ALPHA-FLUOROHYDROCORTISONE ON BLOOD PRESSURE, PLASMA VOLUME, AND SODIUM, POTASSIUM AND WATER BALANCE IN RATS

1974 ◽  
Vol 76 (3) ◽  
pp. 539-555 ◽  
Author(s):  
D. Haack ◽  
E. Hackenthal ◽  
E. Homsy ◽  
B. Möhring ◽  
J. Möhring
Keyword(s):  
Blood Pressure ◽  
Water Balance ◽  
Plasma Volume ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Urinary Sodium ◽  
Blood Pressure Elevation ◽  
High Doses ◽  
Water And Sodium Excretion

ABSTRACT In normal rats on a standard sodium diet, the administration of 9-alpha-fluorohydrocortisone (9aFF) induced a rapid increase of blood pressure in parallel to an increase of plasma volume. Water and potassium balances became negative. Urinary sodium excretion remained unchanged or increased after high doses, whereas urinary sodium concentration and faecal sodium excretion were reduced. The diurnal rhythm of water and sodium excretion changed: during the night-period, renal water and sodium excretion were diminished, whereas during the day-period both were enhanced. Thus, some effects of 9aFF on electrolyte and water balance are similar to those of DOC, while other effects are similar to those of cortisone. It is postulated that a shift of fluid from intracellular to extracellular compartments, which increases plasma volume, is of critical importance for the 9aFF-induced blood pressure elevation in rats.

Lack of evidence for gastrointestinal control of sodium excretion in unanesthetized rabbits

1981 ◽  
Vol 240 (2) ◽  
pp. F94-F100
Author(s):  
L. F. Obika ◽  
E. M. Fitzgerald ◽  
S. D. Gleason ◽  
A. Zucker ◽  
E. G. Schneider
Keyword(s):  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Urinary Sodium ◽  
Plasma Sodium ◽  
Nacl Solution ◽  
Receptor System ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Access To Food

Experiments were performed to determine whether unanesthetized rabbits exhibit a greater natriuresis after oral administration of a hypertonic sodium chloride solution (1.5 mmol NaCl/kg) than after the intravenous administration of the same solution. Male rabbits (New Zealand) were placed on a low sodium diet for 4 days, and on the fifth day a hypertonic NaCl solution (616 mM) was given either by stomach tube (GI) or intravenously (IV), while an equal volume of a hypotonic NaCl solution (31 mM) was given by the alternate route. The studies were repeated on each rabbit so that paired observations were obtained. No differences in plasma Na concentration, peripheral hematocrit, or urinary sodium excretion were observed between the GI and IV groups after administration of the hypertonic NaCl solution. In seven rabbits that were permitted access to food and water following NaCl administration by either route, urinary sodium excretion tended to be reduced (P = 0.08), but, again, no significant differences in plasma sodium concentration, peripheral hematocrit, or urinary sodium excretion were observed between the GI and IV routes of sodium administration. Accordingly, we could find no evidence to support the existence of a GI or portal Na receptor system that regulates urinary sodium excretion in the unanesthetized rabbit.

Multiple, random spot urine sampling for estimating urinary sodium excretion

2021 ◽  
Author(s):  
Gianluigi Ardissino ◽  
Antonio Vergori ◽  
Cesare Vergori ◽  
Laura Martelli ◽  
Valeria Daccò ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Spot Urine ◽  
Urine Sampling

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 Urinary sodium excretion and the risk of cardiovascular disease: A community-based cohort study in Taiwan

2021 ◽  
pp. 1-42
Author(s):  
Yi-Jie Wang ◽  
Kuo-Lioug Chien ◽  
Hsiu-Ching Hsu ◽  
Hung-Ju Lin ◽  
Ta-Chen Su ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Systolic Blood Pressure ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Salt Sensitivity ◽  
Urinary Sodium ◽  
Mediating Effect ◽  
Cvd Risk ◽  
Media Thickness

Abstract Urinary sodium excretion is a potential risk factor for cardiovascular diseases (CVD). However, the underlying biological mechanisms and effects of salt sensitivity are unclear. The purpose of this study was to characterize the relative contribution of biological factors to the sodium-CVD association. A total of 2112 participants were enrolled in this study. Structured questionnaires and blood and urine samples were obtained. Twenty-four-hour sodium excretion was estimated using a single overnight urine sample. Hypertension, metabolic syndrome, and overweight status were considered to indicate salt sensitivity. Cox proportional hazard models were used to investigate the effects of salt sensitivity on urinary sodium excretion and CVD risk. The traditional mediation approach was used to calculate the proportion of mediation. The mean age (standard deviation) of the 2112 participants was 54.5 (12.2) years, and they were followed up for a mean of 14.1 [8.1] years. Compared with those in the lowest quartile, the highest baseline urinary sodium excretion (>4.2g/24 hours) was associated with a 43% higher CVD risk (hazard ratio, 1.43; 95% confidence interval, 1.02-1.99). Participants with high urinary sodium excretion, hypertension, or metabolic syndrome had a significantly high risk of CVD. The carotid intima-media thickness had the largest mediating effect (accounting for 35% of the sodium-CVD association), followed by systolic blood pressure (33%), left ventricular mass (28%), and diastolic blood pressure (14%). Higher urinary sodium excretion increased the risk of CVD, which was explained largely by carotid media-thickness and systolic blood pressure.

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