Sodium excretion patterns during and following intravenous sodium chloride loads in normal and hypertensive pregnancies

1968 ◽  
Vol 102 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Harry E. Sarles ◽  
Sandra S. Hill ◽  
Alvin L. LeBlanc ◽  
Garland H. Smith ◽  
Carlos O. Canales ◽  
...  
Keyword(s):  
Sodium Chloride ◽  
Sodium Excretion ◽  
Intravenous Sodium

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.

Excretion of Salt and Water by Patients with Sickle-Cell Anaemia: Effect of a Diuretic and Solute Diuresis

1977 ◽  
Vol 53 (6) ◽  
pp. 523-527 ◽  
Author(s):  
T. E. Forrester ◽  
G. A. O. Alleyne
Keyword(s):  
Sodium Chloride ◽  
Sickle Cell ◽  
Sodium Excretion ◽  
Chloride Solution ◽  
Sodium Chloride Solution ◽  
Sickle Cell Anaemia ◽  
Ethacrynic Acid ◽  
Free Water ◽  
Loop Of Henle ◽  
Water Reabsorption

1. Patients with sickle-cell anaemia were unable to increase free water reabsorption (TcH2O) in response to intravenous hypertonic sodium chloride solution. 2. Ethacrynic acid caused a brisk natriuresis in patients with sickle-cell anaemia but fractional sodium excretion was lower in these patients. 3. These findings could be explained by abnormal function of the loop of Henle.

Contrasting endocrine responses to acute oral compared with intravenous sodium loading in normal humans

1998 ◽  
Vol 274 (1) ◽  
pp. F111-F119 ◽  
Author(s):  
Donald R. J. Singer ◽  
Nirmala D. Markandu ◽  
Martin G. Buckley ◽  
Michelle A. Miller ◽  
Giuseppe A. Sagnella ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Fold Increase ◽  
Early Response ◽  
Dietary Sodium ◽  
High Sodium ◽  
Sodium Loading ◽  
Sodium Load ◽  
Intravenous Sodium ◽  
Oral Sodium

There is evidence in animals and in humans for accelerated natriuresis after oral compared with intravenous sodium loading. To assess the role of atrial natriuretic peptide (ANP) as a contributory mechanism, we compared the hormonal responses to an intravenous sodium load and to the same sodium load taken orally in three separate groups of healthy subjects in balance on low, normal, or high sodium intake. On each diet, there was a trend for an early delay in sodium excretion, followed by increased natriuresis after the oral compared with intravenous sodium load. On all levels of dietary sodium intake, there was a significant (∼2-fold) increase in plasma ANP levels after intravenous saline infusion. There was a significant suppression of the renin system both after oral and intravenous sodium loading. However, there was no acute increase in plasma ANP levels after the oral sodium load, except on the very low sodium intake. This striking and unexpected observation suggests that changes in plasma ANP levels appear to play little role in the early response to an acute oral sodium load in subjects with sodium intake in the range of 150–350 mmol/day. Endocrine mechanisms for the accelerated increase in sodium excretion after oral compared with intravenous sodium loading remain to be elucidated.

scholarly journals PENDRIN REDUCTION IS ASSOCIATED WITH ACUTE INTRAVENOUS SODIUM CHLORIDE LOADING IN PATIENTS WITH PRIMARY ALDOSTERONISM

2021 ◽  
Vol 39 (Supplement 1) ◽  
pp. e34
Author(s):  
Aihua Wu ◽  
Martin J. Wolley ◽  
Qi Wu ◽  
Diane Cowley ◽  
Richard D. Gordon ◽  
...  
Keyword(s):  
Sodium Chloride ◽  
Primary Aldosteronism ◽  
Sodium Chloride Loading ◽  
Intravenous Sodium

The Relation between the Urinary Excretion of Inorganic Phosphate and Sodium

1971 ◽  
Vol 41 (3) ◽  
pp. 249-256 ◽  
Author(s):  
M. Fulop ◽  
P. Brazeau
Keyword(s):  
Glomerular Filtration Rate ◽  
Sodium Chloride ◽  
Urinary Excretion ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Inorganic Phosphate ◽  
Filtration Rate ◽  
Tubular Reabsorption ◽  
Back Pressure

1. The relation between the urinary excretion of inorganic phosphate and sodium was studied in anaesthetized dogs subjected to acute unilateral increases of ureteral back-pressure while receiving infusions of iso-osmotic sodium chloride. Under these circumstances modest increases of ureteral back-pressure, +14 to +23 cmH2O, were associated with relatively small changes of glomerular filtration rate from control values (−12.7 to +8.2%). 2. Increased ureteral back-pressure caused closely proportionate decreases of urinary phosphate and sodium excretion regardless of whether glomerular filtration rate increased, decreased or remained unchanged. When glomerular filtration rate increased or remained stable, the decreases of phosphate and sodium excretion were attributable to closely proportionate increases of tubular reabsorption of sodium and of phosphate. The increased tubular reabsorption of phosphate may be causally related to the increased tubular reabsorption of sodium.

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