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.

Effectiveness of the aldosterone-sodium and -potassium feedback control system

1976 ◽  
Vol 231 (3) ◽  
pp. 945-953 ◽  
Author(s):  
DB Young ◽  
RE McCaa ◽  
UJ Pan ◽  
AC Guyton
Keyword(s):  
Feedback Control ◽  
Potassium Concentration ◽  
Extracellular Fluid ◽  
Plasma Potassium ◽  
Sodium Concentration ◽  
Feedback Mechanism ◽  
Fluid Volume ◽  
The Body ◽  
Plasma Sodium ◽  
Aldosterone Secretion

This study was conducted to determine the quantitative importance of the aldosterone feedback mechanism in controlling each one of three major factors that have often been associated with aldosterone, namely, extracellular fluid sodium concentration, extracellular fluid potassium concentration, and extracellular fluid volume. To do this, the ability of the body to control these three factors in the face of marked changes in daily sodium or potassium intake was studied under two conditions: 1) in the normal dog, and 2) in the dog in which the aldosterone feedback mechanism was prevented from functioning by removing the adrenal glands and then providing a continuous fixed level of supportive aldosterone and glucocorticoids during the low and high electrolyte intake periods. Under these conditions, removal of feedback control of aldosterone secretion decreased the effectiveness of plasma potassium control by nearly fivefold (39% vs. 8% change in plasma potassium concentration), fluid volume by sixfold (12% vs. 2% change in sodium space) and had no effect on control of plasma sodium concentration (2% change with and without feedback control of aldosterone secretion.)

Synthesis and renal activity of rat atrial granules depend on extracellular volume

1984 ◽  
Vol 247 (4) ◽  
pp. R750-R752
Author(s):  
U. Ackermann ◽  
T. G. Irizawa
Keyword(s):  
Atrial Natriuretic Factor ◽  
Extracellular Volume ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Deoxycorticosterone Acetate ◽  
Natriuretic Factor ◽  
Specific Granules ◽  
Atrial Specific Granules ◽  
Natriuretic Effect

Extracellular fluid volume (by 22Na) and extent of 4-h [3H]fucose incorporation into atrial-specific granules were measured in deoxycorticosterone acetate (DOCA)/salt-loaded or Na-deficient rats. The natriuretic potency of extracts from their atria was also measured in assay rats. DOCA/salt-treated animals had a significantly greater extracellular volume, a significantly greater degree of fucose uptake, and a significantly more potent diuretic and natriuretic effect than did Na-deficient rats. These observations, together with the known decrease in atrial granularity with DOCA treatment, suggest that a chronic increase in extracellular fluid volume is associated with increased synthesis and metabolism of atrial natriuretic factor. They also confirm the finding reported by others that granularity and natriuretic potency are not always directly related. It may be that visible granules represent a peptide storage form that requires further processing to become natriuretic.

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.

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.

Dehydration in Infancy: Hospital Treatment

1989 ◽  
Vol 11 (5) ◽  
pp. 139-143
Author(s):  
Harold E. Harrison
Keyword(s):  
Body Weight ◽  
Intestinal Obstruction ◽  
Plasma Volume ◽  
Potassium Concentration ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Hospital Treatment ◽  
Severe Dehydration ◽  
Physiologic Function

Dehydration of a degree severe enough to require intravenous replacement of water and electrolytes indicates (1) depletion of extracellular fluid sodium and water to such an extent that reduction of plasma volume results or (2) distortion of the composition of extracellular fluid with consequent disturbance of physiologic function. Such distortion may be marked hypernatremia, severe depletion of extracellular bicarbonate, or disturbances of potassium concentration resulting in either hyperkalemia or hypokalemia. In addition, hypocalcemia or hypomagnesemia may require specific replacement of these ions. EXTRACELLULAR FLUID DEPLETION WITH HYPOVOLEMIA The most important cause of extracellular fluid depletion in terms of frequency is loss of gastrointestinal secretions through either diarrhea or vomiting. In persons with lower intestinal obstruction, sequestration of gastrointestinal secretions in dilated loops of intestine may be sufficient to cause dehydration in the absence of vomiting. In infants with diarrhea, the onset of vomiting usually is an indication for intravenous replacement of electrolyte and water deficits. Oliguria is also an important item of information, indicating that dehydration is severe enough to require parenteral fluids. It has been estimated that hypovolemia and reduced glomerular filtration with oliguria results when about one third of extracellular fluid volume has been lost. In an infant, the normal extracellular fluid volume is 25% of body weight; therefore, a loss of 8% of body weight as extracellular fluid would result in the manifestation of severe dehydration with reduction of plasma volume.

Effects of Aprotinin on Renal Function and Urinary Prostaglandin Excretion in Conscious Rats after Acute Salt Loading

1979 ◽  
Vol 56 (6) ◽  
pp. 547-553 ◽  
Author(s):  
H. J. Kramer ◽  
T. Moch ◽  
L. Von Sicherer ◽  
R. Düsing
Keyword(s):  
Renal Function ◽  
Arterial Pressure ◽  
Prostaglandin E2 ◽  
Volume Expansion ◽  
Extracellular Fluid ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Salt Loading ◽  
Expansion Phase ◽  
Conscious Rats

1. Aprotinin, a potent kallikrein inhibitor, was given to conscious rats with and without expansion of the extracellular fluid volume with isotonic saline. 2. In noa-expanded rats aprotinin had no effect on arterial pressure, glomerular filtration rate (GFR), hippuran clearance, urinary flow rate, absolute sodium and potassium excretion or free-water clearance. 3. In volume-expanded rats aprotinin significantly reduced GFR, hippuran clearance, urine volume (V) UNaV, UKV and Cwater/GFR without effect on systemic arterial pressure. 4. Urinary immunoreactive prostaglandin E2 excretion significantly increased during the expansion phase but returned to below the control range during stable extracellular fluid volume expansion. 5. Aprotinin significantly suppressed urinary immunoreactive prostaglandin E2 excretion in non-expanded rats and in volume-expanded rats during the expansion phase, but not during stable expansion. 6. The results suggest that the kallikrein-kinin system may contribute to changes in renal function during extracellular volume expansion. This action may not necessarily be associated with changes in renal prostaglandin E2 activity.

Renal endothelial and macula densa NOS: integrated response to changes in extracellular fluid volume

1999 ◽  
Vol 276 (6) ◽  
pp. R1551-R1561 ◽  
Author(s):  
Branko Braam
Keyword(s):  
Nitric Oxide ◽  
Renal Function ◽  
Perfusion Pressure ◽  
Extracellular Fluid ◽  
Macula Densa ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Sodium Balance ◽  
Integrated Response ◽  
Distal Delivery

If, only 20 years ago, anyone had postulated that the absence of nitric oxide gas (NO) would lead to severe hypertension and destruction of the vascular bed of the kidney within weeks, it is not unlikely that smiles of pity would have appeared on the faces of fellow researchers. By now, this has become common knowledge, and hundreds of reports have appeared on the regulation of vascular and renal function by nitric oxide. The amount of information complicates the design of a concept on how NO participates in control of extracellular fluid volume (ECFV) by the kidney. This review analyzes the function of endothelial and macula densa NO synthase (NOS) in the regulation of renal function. From this analysis, endothelial NOS (eNOS)-derived NO is considered a modulator of vascular responses and of renal autoregulation in particular. Increases in renal perfusion pressure and sodium loading will increase eNOS activity, resulting in vasodilatation and depression of tubuloglomerular feedback system responsiveness. Endothelium-derived NO seems important to buffer minute-to-minute variations in perfusion pressure and rapid changes in ANG II activity. In contrast, macula densa NOS is proposed to drive adaptations to long-term changes in distal delivery and is considered a mediator of renin formation. Increases in perfusion pressure and distal delivery will depress the activity and expression of the enzyme that coincides with, and possibly mediates, diminished renin activity. Together, the opposite responses of eNOS and macula densa NOS-derived NO to changes in ECFV lead to an appropriate response to restore sodium balance. The concept that the two enzymes with different localizations in the kidney and in the cell are producing the same product, displaying contrasting responses to the same stimulus but nevertheless exhibiting an integrated response to perturbation of the most important regulated variable by the kidney, i.e., the ECFV, may be applicable to other tissues.

Urinary system

2011 ◽  
pp. 473-511
Keyword(s):  
Renal Function ◽  
Urinary Tract ◽  
Glomerular Filtration ◽  
Extracellular Fluid ◽  
Body Fluids ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Urinary System ◽  
System P ◽  
Tubular Transport

Urinary tract morphology The kidney 474 The ureters 478 The bladder 480 Histology of the urinary tract 482 Renal function Glomerular filtration 486 Tubular transport 490 Dilute and concentrated urines 494 Regulation of tubule function 496 Diuretics 498 Regulation of body fluids Regulation of extracellular fluid volume and osmolarity ...

Sign in / Sign up

Export Citation Format

Share Document