Vasopressin administration in the first month of life: Effects on growth and water metabolism in hypothalamic diabetes insipidus rats

1977 ◽  
Vol 6 (5) ◽  
pp. 505-509 ◽  
Author(s):  
William A. Wright ◽  
Charles L. Kutscher
PEDIATRICS ◽  
1955 ◽  
Vol 15 (3) ◽  
pp. 298-372
Author(s):  
William B. Macdonald

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.


1984 ◽  
Vol 106 (1) ◽  
pp. 52-55 ◽  
Author(s):  
F. A. László ◽  
S. Csáti ◽  
L. Baláspiri

Abstract. The effect of [1-(β-mercapto-β,β-cyclopentamethylene-propionic acid),2-0-ethyltyrosine,4-valine]-arginine vasopressin on the water metabolism was studied in rats. The compound decreases the antidiuretic action of exogenous vasopressin in Brattleboro rats; in rats without diabetes insipidus it causes temporary polyuria and eliminates the response of antidiuresis to an osmotic stimulus. The results indicate that this compound can block the antidiuretic action of both exogenous and endogenous vasopressin.


1976 ◽  
Vol 81 (3) ◽  
pp. 697-706 ◽  
Author(s):  
G. J. Boer ◽  
F. W. van Leeuwen ◽  
D. F. Swaab ◽  
J. W. L. Nolten

ABSTRACT The acid phosphatase activity of the rat neurohypophysis was measured during increased gonadotrophic hormone levels, in diabetes insipidus (DI) (Brattleboro strain) and after water loading, i. e. conditions that interfere with the function of the hypothalamo-neurohypophyseal system (HNS). In addition determinations of tissue protein, lipid and DNA and of water metabolism were performed. Neurohypophyseal acid phosphatase activity expressed on a dry weight basis increased under all conditions. For gonadectomized females, Brattleboro rats and water loaded males an increased water metabolism was observed. The increased acid phosphatase activity is interpreted as being related to disposal of release residues during stimulation of the HNS (increased gonadotrophic hormone levels and DI) and to disposal of neurosecretory material during inhibition (water loading).


1969 ◽  
Vol 61 (4) ◽  
pp. 720-728 ◽  
Author(s):  
John W. Bauman ◽  
C. Van Wegen ◽  
J. Weil-Malherbe

ABSTRACT To re-examine the relative roles of the anterior and posterior pituitary hormones in diabetes insipidus, the effects of hypophysectomy and hormone replacement therapy in hereditary diabetes insipidus rats (Brattleboro strain) was compared with effect of similar treatment of rats without diabetes insipidus. In agreement with experiments on surgically induced diabetes insipidus, hypophysectomy sharply reduced water intake in rats with hereditary diabetes insipidus (DI rats). Water intake remained considerably higher, however, in these rats than in the non-DI rats following hypophysectomy. ADH treatment reduced water intake nearly to levels seen in non-DI rats. In water deprivation studies it was found that urine concentrating ability of the hypophysectomized non-DI rats was almost twice that of the hypophysectomized DI rats. None of the hormones tested restored water turnover of the hypophysectomized DI rats to that seen in sham operated controls. ACTH and T3 increased water intake, but not to levels seen in DI rats with intact pituitary glands. These experiments lead us to concur with those who hold that maximal flow in diabetes insipidus requires the participation of the anterior pituitary hormones. In addition these experiments indicate that ADH or ADH like material is physiologically functional in hypophysectomized rats (other than the Brattleboro strain), and that its presence accounts for the absence of diabetes insipidus following pituitary removal.


1965 ◽  
Vol 43 (5) ◽  
pp. 699-705 ◽  
Author(s):  
Sydney M. Friedman ◽  
Constance L. Friedman

Salt and water metabolism and the distribution of Na, K, and water in gastrocnemius and in aorta were measured in spontaneous hereditary hypothalamic and in surgically induced diabetes insipidus in the rat. The degree of severity in the two types of the disease was estimated in terms of salt and water handling. Water turnover in 24 hours was about equal to body weight in the hereditary disease and about 60% of body weight in the induced disease. Skeletal muscle Na increased more than 20% in the familial disease, and the gain involved both cells and environment. There was no corresponding loss of K. Similar changes of lesser degree were noted in the induced disease. The degree of Na accumulation appears to be partially dependent on the duration of the disease.


1972 ◽  
Vol 69 (3) ◽  
pp. 434-444 ◽  
Author(s):  
D. V. Naik

ABSTRACT Three genotypes of mice, VII Os/+, DI +/+ and DI Os/+, with nephrogenic (vasopressin resistant) diabetes insipidus (DI) are compared to a normal VII +/+ strain with respect to water intake, urine output, urine osmolality, urine sodium and potassium, and the extractable vasopressor (ADH) activity from the neurohypophysis. From the results obtained, it is confirmed that the severely diabetic DI Os/+ mice produce large volumes of dilute, hypotonic urine and have a 2½ fold vasopressor increase as compared to normal VII +/+ mice, whereas, the mildly diabetic VII Os/+ and DI +/+ stand in between the DI Os/+ and VII +/+ with intermediate volumes of hypertonic urine and a vasopressor increase of 1⅓ and 1½ fold respectively. Further, a parallelism between the severity of diabetes insipidus and increased vasopressor activity is demonstrated in this study. The total excretion of sodium in the urine of VII Os/+ and DI Os/+ is higher than that of the VII +/+ and DI +/+ mice. This natriuresis is associated with Os gene and furthermore, its possible hypothalamic involvement is discussed. The increase of ADH in these hereditary nephrogenic diabetes insipidus mice is a new syndrome and the possible role of other factors involved is discussed.


1987 ◽  
Vol 115 (3) ◽  
pp. 392-398 ◽  
Author(s):  
Ferenc Laczi ◽  
Ferenc A. László ◽  
Gábor L. Kovács ◽  
Gyula Telegdy ◽  
Anna Szász ◽  
...  

Abstract. Intranasal treatment with desglycinamide9-(Arg8)-vasopressin (DGAVP) improved certain aspects of cognitive functions of patients with acquired and congenital diabetes insipidus and of alcoholic patients with mild cognitive impairments. Patients with Korsakoff's syndrome, presenting with severe cognitive impairments, were resistent to DGVP treatment. DGAVP treatment did not affect blood pressure and water metabolism. The action of DGAVP on cognitive functions is probably mediated by centrally located target sites and may be expressed only in patients in whom these target sites are unimpaired.


1960 ◽  
Vol 199 (1) ◽  
pp. 35-38 ◽  
Author(s):  
Sydney M. Friedman ◽  
Constance L. Friedman ◽  
Miyoshi Nakashima

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.


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