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

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.

1978 ◽  
Vol 28 ◽  
pp. 179
Author(s):  
Toshiaki Kadokawa ◽  
Kanno Hosoki ◽  
Kunihiko Takeyama ◽  
Hisao Minato ◽  
Masanao Shimizu

1996 ◽  
Vol 80 (6) ◽  
pp. 1993-2001 ◽  
Author(s):  
F. Bouzeghrane ◽  
S. Fagette ◽  
L. Somody ◽  
A. M. Allevard ◽  
C. Gharib ◽  
...  

To determine the effect of hindlimb suspension on body fluid volume, salt and water balance, and relevant hormones, two series of experiments were performed in an experimental protocol including periods of isolation (7 days), horizontal attachment (7 days), and suspension (14 days). 1) During the first experiment, water and electrolyte balance, arginine vasopressin (AVP), and guanosine 3',5'- cyclic monophosphate (cGMP) were determined in urine, atrial natriuretic peptide in plasma and atria, and renin concentration and AVP in plasma in 30 rats. 2) During the second experiment, blood volume and extracellular fluid volume were measured by a dilution technique (Evans blue and sodium thiocyanate) in another 30 rats. We observed a pronounced and early effect of horizontal attachment on the renal variables. After 48 h, diuresis (49%), natriuresis (44%), kaliuresis (36%), osmotic load (39%), creatinine (28%), and AVP excretion (155%) were significantly increased in attached rats (P < 0.05). There was no short-term (24-h) effect of suspension on urine flow and Na+, K+, creatinine, and AVP excretion, but the urine cGMP decreased significantly (45%; P < 0.05). Significant decreases in natriuresis, kaliuresis, urine creatinine, and osmotic load occurred in the suspension group 7 days after suspension. After the 14-day tail suspension, plasma volume and extracellular fluid volume measured in suspended rats were not different from isolated rat values, whereas plasma volume increased by 15% (P < 0.05) in the attached rats. Plasma immunoreactive plasma atrial natriuretic levels of suspended rats were significantly reduced by 35% vs. isolated rats (P < 0.001) and by 18% vs. attached rats (P < 0.05). By using this experimental protocol, the physiological alterations revealed that suspension produced some acute and long-term effects, but the fixation to the suspension device, restraint, and confinement have their own influence on fluid distribution and renal function.


2004 ◽  
Vol 1 (2) ◽  
pp. 131-139 ◽  
Author(s):  
Michael I Lindinger ◽  
Gloria McKeen ◽  
Gayle L Ecker

AbstractThe purpose of the present study was to determine the time course and magnitude of changes in extracellular and intracellular fluid volumes in relation to changes in total body water during prolonged submaximal exercise and recovery in horses. Seven horses were physically conditioned over a 2-month period and trained to trot on a treadmill. Total body water (TBW), extracellular fluid volume (ECFV) and plasma volume (PV) were measured at rest using indicator dilution techniques (D2O, thiocyanate and Evans Blue, respectively). Changes in TBW were assessed from measures of body mass, and changes in PV and ECFV were calculated from changes in plasma protein concentration. Horses exercised by trotting on a treadmill for 75–120 min incurred a 4.2% decrease in TBW. During exercise, the entire decrease in TBW (mean±standard error: 12.8±2.0 l at end of exercise) could be attributed to the decrease in ECFV (12.0±2.4 l at end of exercise), such that there was no change in intracellular fluid volume (ICFV; 0.9±2.4 l at end of exercise). PV decreased from 22.0±0.5 l at rest to 19.8±0.3 l at end of exercise and remained depressed (18–19 l) during the first 2 h of recovery. Recovery of fluid volumes after exercise was slow, and characterized by a further transient loss of ECFV (first 30 min of recovery) and a sustained increase in ICFV (between 0.5 and 3.5 h of recovery). Recovery of fluid volumes was complete by 13 h post exercise. It is concluded that prolonged submaximal exercise in horses favours net loss of fluid from the extracellular fluid compartment.


1972 ◽  
Vol 43 (2) ◽  
pp. 165-170 ◽  
Author(s):  
P. Sederberg-Olsen ◽  
H. Ibsen

1. In ten patients with essential hypertension treated with propranolol (320 mg daily for 4 months) plasma volume and extracellular fluid volume were determined. 2. A significant increase in extracellular fluid volume (ECFV) was found, but there was no significant change in plasma volume. 3. The genesis of the increase found in ECFV is briefly discussed.


1988 ◽  
Vol 66 (6) ◽  
pp. 1365-1370 ◽  
Author(s):  
M. R. Hughes ◽  
J. R. Roberts

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.


1960 ◽  
Vol 198 (1) ◽  
pp. 148-152 ◽  
Author(s):  
Sydney M. Friedman ◽  
Miyoshi Nakashima ◽  
Constance L. Friedman

Hydrochlorothiazide causes a marked loss of Na and of water in both fully alimented rats and in rats deprived of food and/or water. The increased urinary volume corresponds closely to the shrinkage of the extracellular fluid volume (inulin space) but the decrease in extracellular Na is not sufficient to account for the Na excretion, suggesting that Na is withdrawn from cells and perhaps bone stores as well. The fall in blood pressure in hypertensive rats is not due to simple shrinkage of the extracellular space and plasma volume, but can be referred to the rise in Na gradient induced by withdrawal of cell sodium.


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