Water and solute balance in rats during 10 h water deprivation and rehydration

1993 ◽  
Vol 71 (5-6) ◽  
pp. 379-386 ◽  
Author(s):  
Guus H. M. Schoorlemmer ◽  
Mark D. Evered
Keyword(s):  
Water Balance ◽  
Water Deprivation ◽  
Extracellular Fluid ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Sodium Concentration ◽  
Sodium Balance ◽  
Electrolyte Excretion ◽  
Fluid Deficit

Rats with bladder and venous cannulas were deprived of water from midnight (00:00) to 10:00. Water deprivation reduced food intake within 2 h, reducing the amount of water sequestered in the gut and the solute load to the tissues. There was little change in either urinary water loss or osmolality, but water-deprived rats excreted more Na+, K+, and Cl− than food-matched controls. The change in solute balance helped preserve osmolality and cell volume at the expense of extracellular fluid volume. When water was returned, rats quickly drank enough to restore the intracellular but not the extracellular fluid deficit. Plasma osmolality and sodium concentration fell below predeprivation values. Urine osmolality and excretion of Na+, K+, and Cl− fell rapidly after drinking. Drinking continued at a slower rate for at least 4 h, but urine flow also increased so water balance stabilized. The changes in intake and electrolyte excretion during water deprivation and rehydration illustrate the important role of changes in solute balance in fluid homeostasis.Key words: water deprivation, thirst, drinking, water balance, sodium balance.

Renal effects of overhydration during vasopressin infusion in conscious dogs

1984 ◽  
Vol 247 (1) ◽  
pp. F103-F109 ◽  
Author(s):  
P. Bie ◽  
M. Munksdorf ◽  
J. Warberg
Keyword(s):  
Plasma Protein ◽  
Renal Excretion ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Sodium Concentration ◽  
Conscious Dogs ◽  
Electrolyte Excretion ◽  
Water Load ◽  
Plasma Vasopressin ◽  
Small Doses

The antidiuretic and possibly natriuretic effects of small doses of vasopressin (AVP) were investigated in conscious dogs. Plasma composition and renal excretion of water, Na+, and K+ were measured after overhydration by 20 ml/kg performed during infusion of AVP at rates of 50, 100, 150, 200, or 400 pg X min-1 X kg body wt-1 or of 1-desamino-8-D-arginine vasopressin (DDAVP) 50 pg X min-1 X kg body wt-1. Hydration lowered plasma osmolality and sodium concentration by 4.2 +/- 0.3 and 3.8 +/- 0.2%, respectively; plasma protein showed a larger decrease, 8.5 +/- 0.4% (P less than 0.01). Urine osmolality during hydration was 52 +/- 3 mosmol/kg H2O. AVP infusion at 100 pg X min-1 X kg-1 elevated plasma vasopressin by 1.7 +/- 0.3 pg/ml and urine osmolality by 1,049 +/- 152 mosmol/kg H2O and elicited marked natriuresis and kaliuresis but no change in osmolar clearance. During DDAVP infusion urine osmolality was 1,365 +/- 134 mosmol/kg H2O, but electrolyte excretion was indistinguishable from control. It is concluded that 1) AVP is associated with marked natriuresis and kaliuresis even in doses required to prevent water diuresis, 2) DDAVP--although strongly antidiuretic--does not affect electrolyte excretion, and 3) the water load causes disproportionate dilution of plasma protein and osmolality, probably due to protein redistribution.

Successful rescue of severe hypernatraemia (196 mmol/L) by treatment with hypotonic fluid

2007 ◽  
Vol 44 (5) ◽  
pp. 491-494 ◽  
Author(s):  
Jinny Jeffery ◽  
Ruth M Ayling ◽  
Richard J S McGonigle
Keyword(s):  
Oral Fluid ◽  
Fluid Intake ◽  
Case Reports ◽  
Pure Water ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Chronic Renal Impairment ◽  
Hypotonic Fluid

Hypernatraemia over 160 mmol/L is considered to be severe. This case reports a patient who developed extreme hypernatraemia with a serum sodium concentration of 196 mmol/L. The patient was known to have chronic renal impairment and was admitted with acute deterioration of renal function secondary to dehydration. This was considered to be secondary to poor oral fluid intake (related to depression) and lithium-induced nephrogenic diabetes insipidus with salt-losing nephropathy. The patient had a high urinary sodium excretion but was also in a pure water losing state as evidenced by an inappropriately low urine osmolality for the plasma osmolality and was successfully treated with hypotonic intravenous fluid and desmopressin.

Water deprivation-induced drinking in rats: role of angiotensin II

1983 ◽  
Vol 244 (2) ◽  
pp. R244-R248 ◽  
Author(s):  
C. C. Barney ◽  
R. M. Threatte ◽  
M. J. Fregly
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Water Intake ◽  
Water Deprivation ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Renin Activity ◽  
Deprivation Period ◽  
Dependent Component

The role of angiotensin II in the control of water intake following deprivation of water for varying lengths of time was studied. Male rats were deprived of water for 0, 12, 24, 36, or 48 h. Water intakes were measured with and without pretreatment with the angiotensin I-converting enzyme inhibitor, captopril (50 mg/kg, ip). Captopril had no significant effect on water intake following either 0 or 12 h of water deprivation. However, captopril significantly attenuated water intake following 24-48 h of water deprivation with the magnitude of the attenuation increasing as the length of the period of water deprivation increased. Plasma renin activity was significantly increased over control levels after 24-48 h of water deprivation but not after 12 h of water deprivation. Plasma renin activity tended to increase as the length of the water-deprivation period increased. Serum osmolality and sodium concentration were significantly increased over control levels following 12-48 h of water deprivation. Serum osmolality and sodium concentration failed to show any further increases with increasing length of water deprivation beyond the increases following 12 h of water deprivation. The data indicate that the water intake of water-deprived rats can be divided into an angiotensin II-dependent component and angiotensin II-independent component. The angiotensin II-independent component appears to be more important in the early stages of water deprivation whereas the angiotensin II-dependent component becomes more important as the length of the water-deprivation period increases.

Role of renal nerves in sodium depletion-induced salt appetite

1996 ◽  
Vol 271 (3) ◽  
pp. R806-R812 ◽  
Author(s):  
R. L. Thunhorst ◽  
R. F. Kirby ◽  
A. K. Johnson
Keyword(s):  
Enzyme Inhibitor ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Sodium Balance ◽  
Renal Nerves ◽  
Salt Appetite ◽  
Subcutaneous Injections ◽  
Intact Control ◽  
Water And Sodium Excretion

The ingestion of water and 0.3 M NaCl solution and the secretion of key hormones were studied in groups of intact and bilaterally renal-denervated rats after extracellular fluid depletion. Hypovolemia with mild hypotension was produced by subcutaneous injections of the diuretic furosemide (10 mg/kg) followed by injections of the angiotensin-converting enzyme inhibitor captopril (5 mg/kg s.c.). Denervated rats drank significantly less of a concentrated saline solution in response to depletion than intact control rats did, but drank similar amounts of water. Denervated rats finished testing in significantly greater negative water and sodium balance compared with controls. Renal denervation did not impair the secretion of renin and aldosterone or the formation of angiotensin I. The diminished sodium intake of denervated rats is not attributable to reduced water and sodium excretion in response to the hypovolemic protocol. These results indicate that the integrity of the renal nerves is important for the normal elaboration of salt appetite in response to hypovolemia/hypotension.

Sex difference in urinary concentrating ability of rats with water deprivation

1996 ◽  
Vol 270 (3) ◽  
pp. R550-R555 ◽  
Author(s):  
Y. X. Wang ◽  
J. T. Crofton ◽  
J. Miller ◽  
C. J. Sigman ◽  
H. Liu ◽  
...  
Keyword(s):  
Water Deprivation ◽  
Plasma Concentrations ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Ovarian Hormones ◽  
Urine Flow ◽  
The Other ◽  
Consumptive Behavior ◽  
Urinary Concentrating Ability ◽  
Previous Demonstration

Our previous demonstration of sexual dimorphism in the antidiuretic response to exogenous vasopressin prompted us to investigate the response to moderately high levels of endogenous vasopressin stimulated by water deprivation in conscious rats. After 24 h water deprivation, urine flow was significantly higher and urine osmolality lower in females than in males. Plasma concentrations of vasopressin were higher in females than in males after water deprivation, but plasma osmolality did not differ. Gonadectomy, which had no effect in dehydrated males, decreased urine flow and increased urine osmolality in females to levels observed in intact and gonadectomized males. Spontaneous water intake was also measured and found to be lower in males and estrous females than in females in the other phases of the estrous cycle. These observations support the concept that there is a gender difference in the antidiuretic responsiveness to endogenous vasopressin, that this difference is dependent upon the ovarian hormones, and that it may lead to differences in consumptive behavior.

Satiety and inhibition of vasopressin secretion after drinking in dehydrated dogs

1981 ◽  
Vol 240 (4) ◽  
pp. E394-E401 ◽  
Author(s):  
T. N. Thrasher ◽  
J. F. Nistal-Herrera ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Arginine Vasopressin ◽  
Water Deprivation ◽  
Extracellular Fluid ◽  
Plasma Osmolality ◽  
Rapid Decline ◽  
Vasopressin Secretion

The roles of oropharyngeal and gastric factors in satiation and arginine vasopressin (AVP) secretion were examined in water-deprived dogs. Dogs were prepared with chronic gastric fistulas and received six treatments after 24 h of water deprivation: rehydration with H2O or extracellular fluid (ECF) with the fistula closed; rehydration with H2O or ECF with the fistula open; gastric administration of H2O or ECF via the fistula. Drinking occurred immediately after presentation and was always completed by 6 min. At the end of the 60-min period of observation, water was offered in order to assess the degree of satiety. No differences were observed between the volumes of H2O or ECF consumed. However, only absorption of the water drunk produced complete satiety assessed 60 min later. Drinking H2O caused a fall in plasma AVP 6 min before a detectable decline in osmolality and reached water-replete levels by 15 min after drinking. Drinking H2O or ECF plus removal via the fistula and drinking ECF also brought about a rapid decline in plasma AVP without any change in plasma osmolality. Gastric administration of H2O caused a fall in plasma AVP that coincided with the fall in osmolality, and gastric administration of ECF had no effect on plasma AVP. We conclude that oropharyngeal factors account for temporary satiety and the rapid inhibition of vasopressin secretion.

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.

scholarly journals Vasopressin serum levels and disorders of sodium and water balance in patients with severe brain injury

2007 ◽  
Vol 65 (4b) ◽  
pp. 1158-1165 ◽  
Author(s):  
Eliane de Araújo Cintra ◽  
Sebastião Araújo ◽  
Elizabeth M.A.B. Quagliato ◽  
Margaret de Castro ◽  
Antônio Luiz Eiras Falcão ◽  
...  
Keyword(s):  
Brain Injury ◽  
Water Balance ◽  
Laboratory Data ◽  
Plasma Osmolality ◽  
Serum Levels ◽  
Sodium Balance ◽  
Severe Brain Injury ◽  
Normal Range ◽  
Post Injury ◽  
Sodium And Water Balance

BACKGROUND: Disorders of water and sodium balance are frequently seen in patients with severe brain injury (SBI), and may worsen their prognosis. PURPOSE: To evaluate vasopressin (AVP) serum levels and sodium and water balance disorders during the first week post-injury in patients with SBI. METHOD: Thirty-six adult patients with SBI (admission Glasgow Coma Scale score < 8) and an estimated time of injury < 72 hours were prospectively studied. Clinical and laboratory data were recorded and AVP was measured in venous blood samples collected on the 1st, 2nd, 3rd and 5th days following inclusion. RESULTS: AVP serum levels remained within the normal range in SBI patients (either traumatic or non-traumatic), although tended to be greater in non-survivor than in survivor patients (p=0.025 at 3rd day). In-hospital mortality was 43% (15/36), and serum sodium and plasma osmolality variabilities were greater in non-survivor than in survivor patients during the observation period (p<0.001). CONCLUSION: AVP serum levels remained within the normal range values in these SBI patients, but those who died have shown higher incidence of abnormal sodium and water balance during the first week post-injury.

Approach to the patient with hyponatraemia

2015 ◽  
Author(s):  
Ewout J. Hoorn ◽  
Robert Zietse
Keyword(s):  
Water Balance ◽  
Extracellular Fluid ◽  
Urine Osmolality ◽  
Brain Cells ◽  
Intravascular Volume ◽  
Urine Sodium ◽  
Rate Of Development ◽  
Electrolyte Disorder ◽  
Water Shift ◽  
Balance Disorder

Hyponatraemia is the most common electrolyte disorder in hospitalized patients and is primarily a water balance disorder. Therefore, hyponatraemia is due to a relative excess of water in comparison with sodium in the extracellular fluid volume. Hyponatraemia is usually due to the release of vasopressin despite hypo-osmolality; this secretion is either ‘appropriate’ (i.e. due to a low intravascular volume) or ‘inappropriate’. The diagnostic approach to hyponatraemia relies on the assessment of the time of development, symptoms, and volume status, along with laboratory parameters such as urine sodium and urine osmolality. Complications are mainly neurological and usually depend on the rate of development and correction. If hyponatraemia develops acutely, treatment should be directed towards counteracting the water shift to or brain cells. Conversely, in more chronic cases of hyponatraemia, treatment should be directed at the underlying cause, while avoiding over-correction.

Renal function and sodium balance in conscious Dahl S and R rats

1987 ◽  
Vol 252 (5) ◽  
pp. R833-R841 ◽  
Author(s):  
R. J. Roman ◽  
J. L. Osborn
Keyword(s):  
Sodium Chloride ◽  
Extracellular Fluid ◽  
Free Water ◽  
Urine Osmolality ◽  
High Salt ◽  
Sodium Balance ◽  
Free Water Clearance ◽  
High Salt Diet ◽  
Salt Diet ◽  
Renal Tubular

Renal transplantation studies have indicated that some form of renal dysfunction underlies the development of hypertension in Dahl salt-sensitive (S) rats. In the present study, we compared renal hemodynamic and tubular function of conscious Dahl S and salt-resistant (R) rats. Prehypertensive Dahl S rats had a blunted natriuretic response to an intravenous isotonic sodium chloride load compared with the responses of normotensive Dahl R or hypertensive Dahl S rats. This difference was probably not related to a generalized defect in renal tubular handling of sodium and water, since prehypertensive Dahl S rats excreted quantities of sodium comparable to those of R or hypertensive S rats when infused with hypertonic sodium chloride solutions. Dahl S rats also elevated free water clearance and lowered urine osmolality similar to R rats when challenged with a hypotonic saline load. Renal blood flows and glomerular filtration rates were similar in prehypertensive Dahl S, hypertensive Dahl S, and Dahl R rats. The possible link between sodium retention and the development of hypertension in Dahl S rats was examined further by measuring the changes in sodium and water balance, extracellular fluid volume (ECV), and blood pressure after exposure to an 8% sodium chloride diet. No differences could be detected in the salt and water balances of Dahl S and R rats exposed to a high-salt diet for 14 days. ECV increased significantly by 10% in Dahl S rats on the 1st day of a high-salt diet, whereas no change was observed in Dahl R animals.(ABSTRACT TRUNCATED AT 250 WORDS)

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