Effect of Pitressin on old-age changes of salt and water metabolism in the rat

1960 ◽  
Vol 199 (1) ◽  
pp. 35-38 ◽  
Author(s):  
Sydney M. Friedman ◽  
Constance L. Friedman ◽  
Miyoshi Nakashima
Keyword(s):  
Diabetes Insipidus ◽  
Old Age ◽  
Water Deprivation ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Age Changes ◽  
Water Metabolism ◽  
Parallel Increase ◽  
Daily Urine ◽  
Old Rats

Extracellular fluid volume is characteristically increased in old rats. This is accompanied by a parallel increase in extracellular Na but not K. Daily urine volume and, to a lesser degree, daily urinary Na excretion is also increased in old rats even in the presence of severe water deprivation. These changes, together with an increase in adrenal size, are similar to those observed in diabetes insipidus in the rat. Daily treatment with Pitressin tannate, tested at only one dose level, tended to restore the relevant values towards those of younger normals.

THE USE OF CHLORPROPAMIDE IN DIABETES INSIPIDUS IN CHILDREN

PEDIATRICS ◽  
1970 ◽  
Vol 45 (2) ◽  
pp. 236-245
Author(s):  
Robert M. Ehrlich ◽  
Sang Whay Kooh
Keyword(s):  
Diabetes Insipidus ◽  
Water Deprivation ◽  
Plasma Insulin ◽  
Urine Volume ◽  
Insulin Response ◽  
Urine Osmolality ◽  
Post Traumatic ◽  
Term Management ◽  
Plasma Insulin Response

Oral chlorpropamide was administered to 17 children with diabetes insipidus (D.I.). The cause of the D.I. was idiopathic, six; histiocytosis, five; craniopharyngioma, three; pinealoma, two, and post-traumatic, one. Twenty-four-hour urine volume and measurements of serum and urine osmolality at the beginning and end of a 7-hour water deprivation test were used to evaluatechlorpropamide therapy. Administration of 150 to 400 mg of chlorpropamide per day by mouth caused a reduction in urine volume in all patients (range 8 to 67%). No change in aldosterone, 17-hydroxycorticoids, or electrolyte excretion was noted. Serum electrolytes and glomerular filtration rate were not affected by therapy. Glucose tolerance and plasma insulin response remained normal in those patients tested. Mild leucine sensitivity without significant change in plasma insulin was induced in four children. During water deprivation, seven patients with secondary D.I. but only one with idiopathic D.I. produced hypertonic urine. Hypoglycemia developed in seven children and is the major hazard of treatment. Long-term management of D.I. has been possible in nine children. Oral chlorpropamide is a useful drug in children with vasopressin-sensitive diabetes insipidus.

CONGENITAL PITRESSIN RESISTANT DIABETES INSIPIDUS OF RENAL ORIGIN

PEDIATRICS ◽  
1955 ◽  
Vol 15 (3) ◽  
pp. 298-372
Author(s):  
William B. Macdonald
Keyword(s):  
Diabetes Insipidus ◽  
Extracellular Fluid ◽  
Male Infant ◽  
Renal Tubules ◽  
Post Mortem ◽  
Water Metabolism ◽  
History Of ◽  
Renal Clearances ◽  
Renal Function Tests ◽  
Renal Origin

1) The history of a male infant who presented soon after birth with features of failure to gain weight, dehydration and pyrexia of obscure origin, has been described. A diagnosis of pitressin resistant diabetes insipidus was made. 2) Renal function tests and post-mortem examination, including microdissection of the kidney, indicates that the basic defect in water metabolism was a functional inability of the distal renal tubules to respond to antidiuretic hormone. 3) Consequent dehydration was insufficient to cause circulatory collapse, but affected renal clearances. 4) There was evidence of increased catabolism and poor protein utilisation. 5) Hyperosmolarity of the extracellular fluid was accompanied by a rise in body temperature, probably due to a depression of sweat gland activity. 6) Post-mortem evidence suggests that infants with pitressin resistant diabetes insipidus should be investigated for cystine storage disease.

scholarly journals Coexistence of central diabetes insipidus and salt wasting: the difficulties in diagnosis, changes in natremia, and treatment.

1996 ◽  
Vol 7 (12) ◽  
pp. 2527-2532
Author(s):  
S Laredo ◽  
K Yuen ◽  
B Sonnenberg ◽  
M L Halperin
Keyword(s):  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Central Diabetes Insipidus ◽  
High Rate ◽  
Salt Wasting ◽  
Positive Balance ◽  
Clinical Tools ◽  
Negative Balance

Both central diabetes insipidus (DI) and a high rate of excretion of sodium (Na) and chloride (Cl) contributed to the development of polyuria and dysnatremia in two patients during the acute postoperative period after neurosurgery. To minimize difficulties in diagnosis and projections for therapy, two available (but not often used) clinical tools were helpful. First, the osmole excretion rate early on revealed the co-existence of central DI and an osmotic diuresis. The osmoles excreted were largely Na salts; after antidiuretic hormone acted, this electrolyte diuresis caused the urine flow rate to be much higher than otherwise anticipated. Interestingly, part of this saline diuresis occurred when the extracellular fluid volume was contracted. The tool to explain the basis for the dysnatremias was a tonicity balance. Hypernatremia, which developed before treatment of central DI, was primarily a result of a positive balance for Na rather than a large negative balance for water. Moreover, hyponatremia that developed once antidiuretic hormone acted was primarily a result of a negative balance for Na; the urine volume was large and its Na concentration was hypertonic. To prevent a further decline in the plasma Na concentration, either the Na concentration in the urine should be decreased by provision of urea or a loop diuretic while replacing all unwanted water and electrolyte losses; alternatively, the fluid infused should have a similar Na concentration and volume as the urine (infuse hypertonic saline).

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 Federal clinical guidelines on diagnosis and treatment of diabetes insipidus in adults

2018 ◽  
Vol 15 (2) ◽  
pp. 56-71 ◽  
Author(s):  
Ivan I. Dedov ◽  
Galina A. Mel'nichenko ◽  
Ekaterina A. Pigarova ◽  
Larisa K. Dzeranova ◽  
Liudmila Y. Rozhinskaya ◽  
...  
Keyword(s):  
Diabetes Insipidus ◽  
Diagnostic Testing ◽  
Urine Volume ◽  
Urine Osmolality ◽  
Average Dose ◽  
Regimen Adherence ◽  
Electrolyte Disturbances ◽  
Daily Urine ◽  
Treatment Of Diabetes ◽  
And Function

We do not recommend population screening for diabetes insipidus (DI) (B3). We recommend to perform diagnostic testing for central diabetes insipidus (CDI) in patients who underwent neurosurgery, after skull and brain trauma, subarchnoid hemorrhage (B3). We recommend excluding thirst impairment during all stages of diagnostic assessment (С3). We recommend excluding DI in cases of persistent hypotonic polyuria: excretion of more than 3 L. or more than 40 mL/kg of urine daily; urine osmolality less than 300 mOsm/kg or urinary specific gravity less than 1004 g/L in all urine samples or during Zimnitsky test (В3). After hypotonic polyuria is confirmed, we recommend excluding of the main causes of nephrogenic diabetes insipidus (NDI) (B3). We recommend simultaneous measurement of urine osmolality and blood osmolality/sodium level in order to confirm DI. Blood hyperosmolality (more than 300 mOsm/kg) and/or hypernatremia with low urine osmolality (less than 300 mOsm/kg) confirms DI (B2). If testing does not reveal these findings, we recommend performing a fluid deprivation test to exclude primary polydipsia (PP) (B2). Desmopressin test is recommended to distinguish CDI and NDI (B2). In cases of CDI we recommend to perform head MRI with contrast (B3). In cases of NDI we recommend assessing renal structure and function and possible electrolyte disturbances (C3). In cases of PP we recommend to refer a patient to psychiatrist (B3). We recommend treating CDI with synthetic vasopressin analogue desmopressin (B1). We recommend an individual approach in choosing desmopressin dosage form (B2). As the initial dose is difficult to predict when starting desmopressin treatment, we recommend titrating the dosage using two approaches: the average dose and as required (C4). We recommend educating the patients to ensure knowledge of the features of various desmopressin dosage forms (C4). To decrease the risk of water intoxication, we recommend educating the patients to the water intake regimen adherence (С4). When CDI is accompanied by thirst impairment, we recommend titrating the dose in a clinical setting, with assessment of blood sodium, bodyweight and/or urine volume (C4).

scholarly journals Federal clinical guidelines on diagnosis and treatment of diabetes insipidus in adults

2018 ◽  
Vol 15 (2) ◽  
pp. 56-71
Author(s):  
Ivan I Dedov ◽  
Galina A Mel'nichenko ◽  
Ekaterina A Pigarova ◽  
Larisa K Dzeranova ◽  
Liudmila Y Rozhinskaya ◽  
...  
Keyword(s):  
Diabetes Insipidus ◽  
Diagnostic Testing ◽  
Urine Volume ◽  
Urine Osmolality ◽  
Average Dose ◽  
Regimen Adherence ◽  
Electrolyte Disturbances ◽  
Daily Urine ◽  
Treatment Of Diabetes ◽  
And Function

We do not recommend population screening for diabetes insipidus (DI) (B3). We recommend to perform diagnostic testing for central diabetes insipidus (CDI) in patients who underwent neurosurgery, after skull and brain trauma, subarchnoid hemorrhage (B3). We recommend excluding thirst impairment during all stages of diagnostic assessment (С3). We recommend excluding DI in cases of persistent hypotonic polyuria: excretion of more than 3 L. or more than 40 mL/kg of urine daily; urine osmolality less than 300 mOsm/kg or urinary specific gravity less than 1004 g/L in all urine samples or during Zimnitsky test (В3). After hypotonic polyuria is confirmed, we recommend excluding of the main causes of nephrogenic diabetes insipidus (NDI) (B3). We recommend simultaneous measurement of urine osmolality and blood osmolality/sodium level in order to confirm DI. Blood hyperosmolality (more than 300 mOsm/kg) and/or hypernatremia with low urine osmolality (less than 300 mOsm/kg) confirms DI (B2). If testing does not reveal these findings, we recommend performing a fluid deprivation test to exclude primary polydipsia (PP) (B2). Desmopressin test is recommended to distinguish CDI and NDI (B2). In cases of CDI we recommend to perform head MRI with contrast (B3). In cases of NDI we recommend assessing renal structure and function and possible electrolyte disturbances (C3). In cases of PP we recommend to refer a patient to psychiatrist (B3). We recommend treating CDI with synthetic vasopressin analogue – desmopressin (B1). We recommend an individual approach in choosing desmopressin dosage form (B2). As the initial dose is difficult to predict when starting desmopressin treatment, we recommend titrating the dosage using two approaches: “the average dose” and “as required” (C4). We recommend educating the patients to ensure knowledge of the features of various desmopressin dosage forms (C4). To decrease the risk of water intoxication, we recommend educating the patients to the water intake regimen adherence (С4). When CDI is accompanied by thirst impairment, we recommend titrating the dose in a clinical setting, with assessment of blood sodium, bodyweight and/or urine volume (C4).

GROWTH AND URINE OSMOLARITY IN YOUNG BRATTLEBORO RATS

1977 ◽  
Vol 75 (2) ◽  
pp. 329-330 ◽  
Author(s):  
H. DLOUHÁ ◽  
J. KŘEČEK ◽  
J. ZICHA
Keyword(s):  
Diabetes Insipidus ◽  
Osmotic Pressure ◽  
Water Deprivation ◽  
Czechoslovak Academy ◽  
Brattleboro Rats ◽  
Urine Osmolarity ◽  
Water Diuresis ◽  
Wistar Strain ◽  
Old Rats ◽  
Academy Of Sciences

Institute of Physiology, Czechoslovak Academy of Sciences, Prague, Czechoslovakia, 142 20 (Received 18 April 1977) If Brattleboro rats, homozygous (DI) and heterozygous (non-DI) for diabetes insipidus are deprived of water, no difference in urinary osmotic pressure can be detected between the two genotypes before 14 days of age Dlouhá, Křeček & Zicha, 1976). This may arise from a shortage of vasopressin in non-DI rats until week 3 after birth, as has been demonstrated in rats of the Wistar strain (Křeček, Dlouhá & Křečková, 1961). We have attempted to detect differences in osmoregulation in DI and non-DI rats before diabetes insipidus is manifest. Samples of urine were obtained from 147 young Brattleboro rats by perineal stimulation. In 10- and 14-day-old animals, all procedures were done at 30 °C. Dehydration was induced in 10-, 14-, 18- and 22-day-old rats by water deprivation for 6 h; water diuresis was induced in 14-, 19-

THE VALUE OF RATS WITH HEREDITARY HYPOTHALAMIC DIABETES INSIPIDUS FOR THE BIOASSAY OF VASOPRESSIN

1967 ◽  
Vol 37 (3) ◽  
pp. 335-344 ◽  
Author(s):  
J. J. JONES ◽  
J. LEE
Keyword(s):  
Arterial Pressure ◽  
Diabetes Insipidus ◽  
Urine Volume ◽  
Urine Flow ◽  
Prolonged Administration ◽  
Urinary Osmolality ◽  
Daily Urine ◽  
Pituitary Glands ◽  
Hereditary Hypothalamic Diabetes Insipidus ◽  
Stimulation Of

SUMMARY The pituitary glands of 11 rats (six females and five males, weighing 140–200g.) with hereditary hypothalamic diabetes insipidus (DI) were found to contain oxytocin but no vasopressin. The DI rats could not always be distinguished from rats without diabetes insipidus (non-diabetes insipidus, NDI rats) by measurement of their daily urine volume. Stimulation of the neurohypophysis by fall in arterial pressure (haemorrhage, methacholine) or by nicotine, released vasopressin in NDI rats to produce a sustained antidiuresis, but in the DI rats there was only a transient fall in urine flow which did not outlast the hypotension. The DI rats were about twice as sensitive to vasopressin as NDI rats. As assay preparations they have the advantage that they cannot respond to vasopressin-releasing stimuli. Prolonged administration of Pitressin tannate in oil increased maximum urinary osmolality in DI rats, but failed to increase their sensitivity to intravenously injected vasopressin.

scholarly journals Congenital nephrogenic diabetes insipidus accompanied with central nephrogenic diabetes secondary to pituitary surgery -a case report

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Wei Zhang ◽  
Yimin Shen ◽  
Yuezhong Ren ◽  
Yvbo Xin ◽  
Lijun Wang
Keyword(s):  
Diabetes Insipidus ◽  
Nephrogenic Diabetes Insipidus ◽  
Direct Detection ◽  
Urine Volume ◽  
Pituitary Surgery ◽  
Accurate Method ◽  
Heterozygous Mutation ◽  
Case Presentation ◽  
Congenital Nephrogenic Diabetes Insipidus

Abstract Background Diabetes insipidus (DI) can be a common cause of polydipsia and polyuria. Here, we present a case of congenital nephrogenic diabetes insipidus (CNDI) accompanied with central diabetes insipidus (CDI) secondary to pituitary surgery. Case presentation A 24-year-old Chinese woman came to our hospital with the complaints of polydipsia and polyuria for 6 months. Six months ago, she was detected with pituitary apoplexy, and thereby getting pituitary surgery. However, the water deprivation test demonstrated no significant changes in urine volume and urine gravity in response to fluid depression or AVP administration. In addition, the genetic results confirmed a heterozygous mutation in arginine vasopressin receptor type 2 (AVPR2) genes. Conclusions She was considered with CNDI as well as acquired CDI secondary to pituitary surgery. She was given with hydrochlorothiazide (HCTZ) 25 mg twice a day as well as desmopressin (DDAVP, Minirin) 0.1 mg three times a day. There is no recurrence of polyuria or polydipsia observed for more than 6 months. It can be hard to consider AVPR2 mutation in female carriers, especially in those with subtle clinical presentation. Hence, direct detection of DNA sequencing with AVPR2 is a convenient and accurate method in CNDI diagnosis.

scholarly journals The physiological and metabolic impacts on sheep and cattle of feed and water deprivation before and during transport

2007 ◽  
Vol 20 (1) ◽  
pp. 17-28 ◽  
Author(s):  
James P. Hogan ◽  
J. Carol Petherick ◽  
Clive J. C. Phillips
Keyword(s):  
Weight Loss ◽  
Recovery Time ◽  
Plasma Cortisol ◽  
Water Deprivation ◽  
Animal Health ◽  
Extracellular Fluid ◽  
Rumen Microbes ◽  
Enteropathogenic Bacteria ◽  
Meat Safety ◽  
Reduced Rate

Sheep and cattle are frequently subjected to feed and water deprivation (FWD) for about 12 h before, and then during, transport to reduce digesta load in the gastrointestinal tract. This FWD is marked by weight loss as urine and faeces mainly in the first 24 h but continuing at a reduced rate subsequently. The weight of rumen contents falls although water loss is to some extent masked by saliva inflow. FWD is associated with some stress, particularly when transportation is added. This is indicated by increased levels of plasma cortisol that may be partly responsible for an observed increase in the output of water and N in urine and faeces. Loss of body water induces dehydration that may induce feelings of thirst by effects on the hypothalamus structures through the renin–angiotensin–aldosterone system. There are suggestions that elevated cortisol levels depress angiotensin activity and prevent sensations of thirst in dehydrated animals, but further research in this area is needed. Dehydration coupled with the discharge of Na in urine challenges the maintenance of homeostasis. In FWD, Na excretion in urine is reduced and, with the reduction in digesta load, Na is gradually returned from the digestive tract to the extracellular fluid space. Control of enteropathogenic bacteria by normal rumen microbes is weakened by FWD and resulting infections may threaten animal health and meat safety. Recovery time is required after transport to restore full feed intake and to ensure that adequate glycogen is present in muscle pre-slaughter to maintain meat quality.

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