Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1 The effect of a combination of chloropropamide and chlorothiazide in Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI) treated with low doses of vasopressin (Pitressin tannate in oil) was investigated with particular reference to the time course of response from the initiation of treatment. 2 Analysis of the relationship between water intake and body weight indicated no real correlation and body weight accounted for only 4.4% of the variation in water intake. It was therefore decided to use whole body responses as the index in preference to the response per unit body weight. 3 The daily administration of 5 mg chlorpropamide combined with chlorothiazide in the drinking water (4 mg/1) to Pitressin-treated DI rats potentiated the response to small doses of vasopressin (25 and 50 mu Pitressin/24 hours). Water intake was reduced by the drug combination by an average of 12.35 ml/24 h, but only on the second day of treatment was the decrease of any real magnitude (30 ml/24 h but otherwise 9 ml/24 h or less). Analysis of urine volume measurements gave similar results to those obtained for water intake and the potency ratio measured in terms of free water clearance was 1.26 (agreeing closely with the ratio for water intake which was 1.24). 4 A reduction in the solute excretion was observed only in those DI rats treated with the higher dose of Pitressin (50 mu/24 h) combined with the two drugs. 5 Possible reasons for the discrepancy between the effect of the combination of chlorpropamide and chlorathiazide on water metabolism in the DI rat and the DI patient are discussed.
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PMID:Potentiation of the response to vasopressin (pitressin) by treatment with a combination of chlorpropamide and chlorothiazide in Brattleboro rats with hereditary hypothalamic diabetes insipidus. 83 92

The food and fluid intake, the fecal weight and weight of urine voided, urinary and plasma osmolality and neurohypophysial content of vasopressin and oxytocin were measured in groups of rats injected with oil and vasopressin (0.5 IU Pitressin tannate in oil daily, i.m.) before, during and after substitution of a 2% solution of NaCl for drinking water for 3 days. Before 2% NaCl was substituted for the drinking water, vasopressin treatment significantly decreased food and water intake (p smaller than 0.05) and daily weight gain (p smaller than 0.01), but no significant effect on plasma osmolality or on neurohypophysial content of vasopressin and oxytocin could be demonstrated. Vasopressin treatment did not significantly reduce the intake of the 2% NaCl solution when this was substituted for drinking water but did reduce the resulting neurohypophysial depletion of vasopressin (p smaller than 0.01). Furthermore, on the first day of NaCl drinking, the neurohypophysial content of vasopressin in vasopressin-treated rats was increased above the control value (p smaller than 0,05). These results suggest the existence of a negative feedback of vasopressin on its own release.
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PMID:Reduced depletion of neurohypophysial hormone stores by vasopressin administration in rats drinking 2% NaCl. 114 33

The postnatal developmental course of the enhanced OT serum level of the vasopressin-deficient (homozygous) Brattleboro rat was investigated radioimmunochemically together with the response to treatment with Pitressin tannate. Compared with heterozygous Brattleboro (control) pups, in which serum OT appeared to have an adult value from birth onwards (about 10 pmol/l), homozygous rats had approximately 2-fold enhanced OT serum level throughout early development. Between day 55 and adulthood the levels of OT rose further to 40-50 pmol/l. A 3-day treatment with Pitressin tannate both in the period before or after the age (day 16) at which the polyuria of the homozygous Brattleboro mutant can be revealed, failed to reduce the serum OT. It was therefore concluded that the high OT serum levels in the vasopressin-deficient Brattleboro rat are not induced by osmotic imbalance, but probably originates from functional teratological aspects of the mutation.
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PMID:Elevated serum oxytocin of the vasopressin-deficient Brattleboro rat is present throughout life and is not sensitive to treatment with vasopressin. 338 37

Brattleboro rats with hereditary hypothalamic diabetes insipidus (BDI) received daily subcutaneous injections of vasopressin in the form of Pitressin tannate (0.5 IU/24 hr). They were initially deprived of food and then trained to work for food reward in a Skinner box to a fixed ratio of ten presses for each pellet received. Once this schedule had been learned the rats were given a discrimination task daily for seven days. The performances of these BDI rats were compared with those of rats of the parent Long Evans (LE) strain receiving daily subcutaneous injections of vehicle (arachis oil). Comparisons were also made between these two groups of treated animals and untreated BDI and LE rats studied under similar conditions. In the initial learning trial, both control and Pitressin-treated BDI rats performed significantly better, and manifested less fear initially, than the control or vehicle-injected LE rats when first placed in the Skinner box. Once the initial task had been learned there was no marked difference in the discrimination learning between control or treated BDI and LE animals. These results support the view that vasopressin is not directly involved in all types of learning behaviour, particularly those involving positively reinforced operant conditioning.
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PMID:Lack of effect of Pitressin on the learning ability of Brattleboro rats with diabetes insipidus using positively reinforced operant conditioning. 407 Mar 91

An attempt was made to prevent the growth impairment of body and brain of the Brattleboro rat congenitally deficient in vasopressin (VP), by postnatal treatment with VP between the ages of 5 and 28 days. Neither repeated daily subcutaneous injections of either Pitressin tannate or VP in oil, continuous peripheral application of VP in various dosage rates using the long-acting Accurel/collodion implantable delivery module, nor daily intracerebroventricular injections of VP in saline, improved postnatal body or brain growth. Brain parts known to be particularly impaired in the Brattleboro neonate, viz. cerebellum and medulla oblongata, also remained unaffected by the VP treatment with regard to both size and cell content as measured on day 33 of age. A possible trophic action of VP would therefore have to take place before neonatal day 5. At dosage rates of VP higher than 1 microgram/d and given peripherally on day 5 or shortly thereafter, a permanent enhancement of diuresis of approximately 30% was noticed in these Brattleboro rats, which were already suffering from a severe diabetes insipidus. Since VP is not circulating at that stage, other systems than the hypothalamo-neurohypophyseal/kidney axis might be affected. Normal antidiuresis obtained following a sub-maximal dosage of Pitressin tannate, indeed showed that the VP receptors of the kidney were still intact. This observation should serve as a warning against application of VP or its analogues during development in clinical practice.
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PMID:Vasopressin fails to restore postnatally the stunted brain development in the Brattleboro rat, but affects water metabolism permanently. 647 54

The effect of [1-(beta-mercapto-beta,beta- cyclopentamethylene -propionic acid)2-0- ethyltyrosine ,4-valine] arginine vasopressin on the water metabolism was studied in rat. The compound was found to be able to block the antidiuretic action of both exogenous and endogenous vasopressin. A rat model of the Schwartz-Bartter syndrome was created by the administration of a high dose of a posterior pituitary preparation (Pitressin tannate ) together with a forced water intake. The antagonist prevented water retention and averted the enhanced natriuresis and hyponatraemia, and cerebral oedema did not develop. The observations suggest that this vasopressin antagonist might be of use in the future as an effective drug against the Schwartz-Bartter syndrome.
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PMID:Effect of the vasopressin antagonist d(CH2)5 Tyr(Et)VAVP on diuresis in rat. 673 24

The effects of fluid intake on basal and vasopressin-responsive urinary PGE excretion (UPGEV) were examined in conscious rats under conditions of 1) ad libitum water intake, 2) water deprivation, and 3) water diuresis induced by ad libitum intake of 5% dextrose in water. UPGEV fell progressively during 40 h of water deprivation. Water diuresis after water deprivation increased UPGEV transiently (8 h). Vasopressin (Pitressin tannate in oil, 5 U/kg subcutaneously) increased UPGEV and decreased urine volume (V) in rats on ad libitum water intake but did not alter UPGEV during water deprivation. Indomethacin suppressed UPGEV (70-90%), increased basal urine osmolality (Uosmol), and potentiated the antidiuretic response to Pitressin in rats on ad libitum water intake. Indomethacin accelerated by 8 h the onset of maximal antidiuresis in water-deprived rats but did not significantly alter water balance. During water diuresis, UPGEV declined in the first 8 h after Pitressin. Thereafter, UPGEV increased markedly, concurrent with early vasopressin escape. Indomethacin or meclofenamate inhibited the rise in UPGEV, the decline in Uosmol, and the increase in V of the escape phase. Indomethacin or meclofenamate also impaired the excretion of an acute water load (5% body wt) given during escape. The spontaneous decline in UPGEV during hydropenia may serve to maximize physiologic antidiuresis. Conversely, the marked increase in UPGEV induced by administration of vasopressin during water diuresis may serve to suppress the antidiuretic response and thus play a role in the mediation of escape from physiologically inappropriate antidiuresis.
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PMID:Effects of fluid intake on basal and vasopressin-responsive urinary prostaglandin E. 686 38

In two-kidney one-clip hypertensive rats we evaluated the effect of water restriction on the development and maintenance of severe hypertension (systemic blood pressure 200-230 mmHg). After application of renal arterial clips in rats allowed access to water for 1 or 2 h daily, BP stabilized at 180-190 mmHg. No increase in water intake occurred and plasma renin activity(PRA) (measured before the drinking period) was significantly below the levels observed in ad libitum-drinking hypertensive rats. In rats administered 4 ml water/100 g body weight twice daily by gavage, development of hypertension was more clearly suppressed. Blood pressure increased slowly and reached levels of only 150-170 mmHg. Furthermore, PRA was significantly lower in this group compared with ad libitum-drinking hypertensive animals. In rats with established (4-5 wk) renal hypertension, restriction of water intake to 1 or 2 h daily resulted in a rapid decrease in BP of about 30 mmHg. Daily administration of Pitressin tannate to hypertensive rats allowed free access to water induced a similar decrease in BP as well as suppression of PRA. These results indicate that the hypotensive effect of water restriction in the two-kidney one-clip hypertensive rat model may be mediated, at least in part, through elevated circulating levels of vasopressin that subsequently inhibit renin release.
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PMID:Hypotensive effect of water restriction in the two-kidney one-clip hypertensive rat. 703 85