Sodium uptake from the gut of freshwater- and seawater-acclimated ducks and gulls

1988 ◽  
Vol 66 (6) ◽  
pp. 1365-1370 ◽  
Author(s):  
M. R. Hughes ◽  
J. R. Roberts
Keyword(s):  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Ion Concentration ◽  
Plasma Sodium ◽  
Salt Glands ◽  
Gut Epithelium ◽  
Seawater Acclimation ◽  
Na Uptake

The first possible regulator of plasma sodium ([Na]pl) and chloride ([Cl]pl) concentrations is the gut epithelium. Its in vivo role in uptake of ingested salt in birds with salt glands has not been evaluated. In the present study the anterior gut 22Na uptake rate was measured in freshwater-acclimated ducks (Anas platyrhynchos) and gulls (Larus glaucescens) and was then measured in the same birds after acclimation to 2/3 seawater. The 22Na was given orally in 7–10 mL of 171 mM NaCl. In ducks, seawater acclimation increased [Na]pl and [Cl]pl but not Na space; in gulls seawater acclimation increased Na space, but not plasma ion concentration. The rate of gut 22Na uptake was the same in ducks and gulls and was not affected by seawater acclimation in either species. As determined from the 22Na distribution between erythrocytes and plasma 3 h after i.v. 22NaCl injection, duck erythrocytes sequestered more (9.3% ± 0.4%) of the load than did gull erythrocytes (6.9% ± 0.3%) (P < 0.001). Although gulls are better hyperosmotic regulators than ducks, there was no difference between the two species in the entry of sodium into the extracellular fluid volume from the gut. Immediately after oral gut loading with dilute saline, freshwater-acclimated gull [Cl]pl, increased more (2P < 0.001) than could be accounted for by equilibration of the administered Cl within the extracellular fluid volume. After gut loading, the increase in [Cl]pl, of freshwater-acclimated ducks was less rapid and could be accounted for by extracellular distribution of the oral Cl load. In seawater-acclimated gulls, [Cl]pl decreased following gut loading, but was unchanged in seawater-acclimated ducks.

scholarly journals Plasma sodium, extracellular fluid volume, and blood pressure in healthy men

2021 ◽  
Vol 9 (24) ◽  
Author(s):  
Jacqueline J. J. O. N. Bosch ◽  
Niek R. Hessels ◽  
Folkert W. Visser ◽  
Jan A. Krikken ◽  
Stephan J. L. Bakker ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Plasma Sodium ◽  
Healthy Men

scholarly journals Comparative Roles of the Renal Apical Sodium Transport Systems in Blood Pressure Control

2000 ◽  
Vol 11 (suppl 2) ◽  
pp. S135-S139
Author(s):  
PIERRE MENETON
Keyword(s):  
Collecting Duct ◽  
Extracellular Fluid ◽  
Pressure Control ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Transport Systems ◽  
Salt Diet ◽  
Fluid Homeostasis ◽  
Low Salt

Abstract.Human genetic studies suggest that the genes encoding renal apical Na+transport proteins play an essential role in the control of extracellular fluid volume and BP. Mice with mutations in each of these genes provide the unique opportunity to directly assess their respective involvement in fluid homeostasis and BP controlin vivo. Inactivation of either the epithelial Na+channel (ENaC) or the Na+-Cl-cotransporter decreases BP to the same extent in mice fed a low-salt diet, despite a more pronounced perturbation of fluid homeostasis in ENaC-deficient mice. In contrast, inactivation of Na+/H+exchanger 3 (NHE3) or the Na+-K+-2Cl-contransporter reduces BP with a normal-salt diet and renders mice unable to survive with a low-salt diet. Therefore, the general conception that ENaC in the collecting duct is the main renal controller of Na+balance and extracellular fluid volume should be tempered. For example, NHE3 in the proximal convoluted tubule seems to play a more substantial role in the control of fluid homeostasis. The overall effect of NHE3 inacthvation on BP may also involve absorptive defects in the intestine and colon, where the exchanger normally reabsorbs significant amounts of Na+and water.

Body compostion in vivo. VIII. Some physiological implications with respect to extracellular fluid volume arising from the distribution of thiocyanate in sheep

1965 ◽  
Vol 16 (4) ◽  
pp. 667 ◽  
Author(s):  
BA Panaretto
Keyword(s):  
Body Weight ◽  
Specific Activity ◽  
Rumen Fluid ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume

The distribution of [35S]-thiocyanate in sheep was studied. The specific activity in rumen fluid during the first 4 hr after injection was markedly less than in serum, and equilibration between rumen fluid and blood was not reached until 20–30 hr after injection. There were large urinary losses of the marker and approximately 50% of the dose was lost in 24 hr. Activity in rumen fluid and urine was due to [35S]-thiocyanate. The thiocyanate spaces, allowing for urinary losses, during the first 4 hr after injection were 25 –30% body weight, increasing to 35–40% body weight at 20–30 hr after injection. The physiological implications of the results with respect to measuring extracellular fluid volume in sheep are discussed.

Plasma Volume, Extracellular Fluid Volume and Exchangeable Sodium Concentrations in the New Zealand Strain of Genetically Hypertensive Rat

1973 ◽  
Vol 44 (4) ◽  
pp. 349-358 ◽  
Author(s):  
C. R. Gresson ◽  
D. L. Bird ◽  
F. O. Simpson
Keyword(s):  
Cardiac Output ◽  
New Zealand ◽  
Plasma Volume ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Plasma Sodium ◽  
Exchangeable Sodium ◽  
Renal Handling ◽  
Volume Percentage

1. Rats of the New Zealand strain with genetic hypertension (GH rats) were found to have lower plasma volume in relation to body weight than rats of the normotensive parent strain (N rats). GH rats had higher venous packed-cell volume percentage than N rats, but total erythrocyte volume was similar in the two strains of rats. Extracellular fluid volume and exchangeable sodium concentrations were lower in the GH rats. Plasma sodium concentration was not altered; plasma potassium concentration was slightly higher in the GH rats. 2. These results indicate that hypersecretion of a sodium-retaining hormone is unlikely to be a primary factor causing hypertension in the GH rats. Cardiac output has not been measured: if an increased cardiac output is a factor in the maintenance of the hypertension, it is evidently not secondary to an increased blood volume. 3. The lower exchangeable sodium concentrations and body fluid volumes found in the GH rats may be due to lower aldosterone activity secondary to a decrease in the activity of the renin-angiotensin system, or to the effects of the elevated blood pressure on the renal handling of sodium, or to both factors.

Separate roles of sodium ion concentration and fluid volumes in salt-loading hypertension in sheep

1975 ◽  
Vol 229 (4) ◽  
pp. 1068-1072 ◽  
Author(s):  
Norman RA ◽  
TG Coleman ◽  
Wiley TL ◽  
Manning RD ◽  
AC Guyton
Keyword(s):  
Extracellular Fluid ◽  
High Volume ◽  
Fluid Volume ◽  
Sodium Ion ◽  
Extracellular Fluid Volume ◽  
Ion Concentration ◽  
Sodium Retention ◽  
Salt Loading ◽  
High Sodium ◽  
Total Nephrectomy

The goal of these studies was to determine whether the hypertension caused by excessive salt loading results from sodium-induced expansion of the extracellular fluid volume or whether the salt increases the pressure in some other way, such as by causing vascular constriction. In one group of sheep, a combination of total nephrectomy and hemodialysis was used to produce and maintain step increases in extracellular fluid volume for 1 wk without a significant change in sodium ion concentration. In a 2nd group, unilateral nephrectomy, dialysis, and DOCA administration were used to cause step increases in sodium ion concentration while the extracellular fluid volume was held as close to normal as possible. The results showed a 41% increase in arterial pressure in the high-volume sheep and only a 4% increase in pressure in the high-sodium sheep. In both instances the total exchangeable sodium increased almost equally--a 21% increase in the high-sodium sheep. The data support the concept that sodium retention causes hypertension almost entirely because of sodium-induced expansion of the extracellular fluid volume.

Extrarenal Factors in Diabetes Insipidus in the Rat

1958 ◽  
Vol 192 (2) ◽  
pp. 401-404 ◽  
Author(s):  
Sydney M. Friedman ◽  
Harald F Scherrer ◽  
Miyoshi Nakashima ◽  
Constance L. Friedman
Keyword(s):  
Renal Function ◽  
Diabetes Insipidus ◽  
Potassium Concentration ◽  
Extracellular Volume ◽  
Extracellular Fluid ◽  
Plasma Potassium ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Plasma Sodium ◽  
Sodium Potassium

Using inulin as indicator of the extracellular volume, the distribution of sodium, potassium and water was studied in rats with diabetes insipidus produced by interrruption of the supraoptico-hypophyseal tract. A well defined increase in the extracellular fluid volume associated with normal plasma sodium and reduced plasma potassium concentration was uniformly present in the rats with diabetes insipidus. These changes occurred in nephrectomized animals and were thus independent of renal function, but were in some degree referable to an increase in adrenal function since they could be partially reversed by adrenal ablation.

scholarly journals Effects of nonsteroidal anti-inflammatory drugs on plasma volume and extracellular fluid volume in rats

1978 ◽  
Vol 28 ◽  
pp. 179
Author(s):  
Toshiaki Kadokawa ◽  
Kanno Hosoki ◽  
Kunihiko Takeyama ◽  
Hisao Minato ◽  
Masanao Shimizu
Keyword(s):  
Plasma Volume ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Inflammatory Drugs ◽  
Anti Inflammatory
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