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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

A double-blind controlled trial of aqueous vasopressin injection (Pitressin) in the prophylaxis of lumbar puncture reactions in 50 patients showed that the incidence of reactions was unaffected, but that severe reactions occurred less frequently in the treatment group. Moderately severe side-effects occurred in 27% of those receiving vasopressin.
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PMID:Vasopressin in prevention of lumbar puncture headache. 488 41

The posterior pituitary gland is considered to be a source of a corticotrophin releasing factor(s) distinct from vasopressin. In this study, the corticotrophin releasing activity of a commercial posterior pituitary extract (Pitressin) and synthetic vasopressin were compared, using a perfused rat pituitary monolayer system. Pitressin was shown to have approximately twice the releasing activity than could be accounted for by its vasopressin content. Fractionation of the posterior pituitary extract, using high pressure liquid chromatography, showed it to contain active material co-eluting with synthetic vasopressin, and at least three other corticotrophin releasing factors. The releasing activity of the most active of these factors was investigated and was found to stimulate ACTH release in a dose-related manner.
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PMID:Studies on the corticotrophin releasing activity of a posterior pituitary extract. 626 79

Synthetic alpha-melanotropin stimulated the release of immunoreactive adrenocorticotropin from primary cultures of rat anterior pituitary cells. The effect of the alpha-melanotropin was dose-dependent. Cells incubated with synthetic arginine-vasopressin and alpha-melanotropin simultaneously produced an amount of adrenocorticotropin that was greater than the sum of the amount that the cells produced in response to each peptide added separately. Other peptides structurally similar to alpha-melanotropin, such as, beta-, gamma 1-, gamma 2-, and gamma 3-melanotropin, were also tested for adrenocorticotropin-releasing activity. Only the gamma 3-melanotropin demonstrated a statistically significant effect. A vasopressin preparation (Pitressin, Parke-Davis) purified from posterior pituitaries and previously shown to contain some alpha-melanotropin was much more potent in releasing adrenocorticotropin than the synthetic vasopressin.
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PMID:Corticotropin-releasing activity of alpha-melanotropin. 627 77

The regulation of sperm transport through the Wolffian duct of male amphibians is poorly understood. These experiments were conducted using rough-skinned newts (Taricha granulosa) to determine if Wolffian ducts are capable of contracting in vitro and, if so, to characterize the contractile responses to acetylcholine (ACh), norepinephrine (NE), and neurohypophysial hormones. Dose-response curves for NE and ACh, which were prepared by measuring isometric contractions, are similar to those reported for mammalian vas deferens. For NE, the minimum effective dose and ED50 were found to be 1 X 10(-5)M and 4.17 X 10(-5)M, respectively. For ACh, the minimum effective dose was 3.2 X 10(-8)M and the ED50 was 1.37 X 10(-5)M. Alpha-adrenoreceptors appear to mediate the contractile responses to NE because phentolamine (10(-5)M) blocked or attenuated the response to NE (10(-6)M, 10(-5)M or 10(-4) M). Beta-adrenoreceptors appear to mediate relaxation because dichloroisoproterenol (10(-5)M) enhanced the response to 10(-5)M NE. The contractile response to three neurohypophysial hormones were also investigated. Arginine vasotocin was more effective in eliciting contractions than oxytocin. The effect of lysine vasopressin was intermediate between arginine vasotocin and oxytocin. These experiments demonstrate that amphibian (Taricha) Wolffian ducts contract in vitro in response to neurotransmitters and neurohypophysial hormones. The contractile response to neurotransmitters occurs in a dose-dependent manner; the response to neurohypophysial hormones is hormone specific.
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PMID:Contractions of amphibian Wolffian duct in response to acetylcholine, norepinephrine, and arginine vasotocin. 630 30

The effect of cold exposure (CE) on renal water excretion has not been clearly delineated. Conscious rats were exposed to decreased ambient temperature (15 degrees C). Forty-five minutes of CE resulted in reversible increases in urine flow and decreases in urine osmolality. The diuresis was not due to a diminished response to vasopressin (VP), as the antidiuresis associated with 500 microU of Pitressin given to water-diuresing rats was comparable at 15 and 30 degrees C. To determine whether the diuresis was due to intrarenal factors, glomerular filtration rate, renal blood flow, sodium excretion, and osmolar clearances were measured and found to be equivalent during control and cold conditions. To determine whether the observed diuresis was due to suppression of endogenous VP, VP-free Brattleboro rats undergoing a constant VP infusion were cold exposed. In these rats, CE was not associated with a change in either urine flow or urinary osmolality. This antidiuretic hormone-mediated mechanism was corroborated by a decrease in immunoassayable VP levels. To determine the mechanism whereby CE suppresses endogenous VP, plasma osmolality and hemodynamic parameters were measured. Although CE was not associated with a change in plasma osmolality, it did result in a significant increase in both mean arterial pressure and cardiac index. Pretreatment of rats with 6-hydroxydopamine prevented both the increase in mean arterial pressure and cold diuresis. We conclude that the diuresis observed upon exposure to 15 degrees C results from nonosmotic suppression of endogenous VP, as a consequence of the increase in mean arterial pressure.
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PMID:Mechanism of cold diuresis in the rat. 640 36

The effect of vasopressin on the lower esophageal sphincter pressure (LESP) is still poorly understood. The present study was designed to determine the effect of I.V. and intra-arterial administration of 8-arginine vasopressin (Pitressin) on the LESP in dogs. A total of 16 anesthetized mongrel dogs were given a continuous perfusion of Pitressin for 20 minutes. Group A (3 dogs): Infused at 2.75 mU/kg/min into the superior mesenteric artery. Group B (3 dogs): 2.75 mU/kg/min into a peripheral vein. Group C (5 dogs): 14 mU/kg/min into a peripheral vein (equivalent to therapeutic dose in humans). Group D (5 dogs): 28 mU/kg/min into a peripheral vein. Esophageal manometry was performed using a triple lumen polyvinyl tube assembly perfused with water at 0.4 ml/min. LESP was checked by the pull-through technique before, immediately and 30 minutes later after termination of the infusion. LESP was monitored at 3 locations during the infusion. No change in LESP was noted when Pitressin (2.75 mU/kg/min) was infused intra-arterial or I.V. I.V. infusion of 14 and 28 mU/kg/min Pitressin caused a significant sustained decrease in LESP (p less than 0.001). After infusion of 28 mU/kg/min, LESP failed to return to control levels in 30 minutes. The results suggest that intravenous administration of a high dose of Pitressin predisposes to gastroesophageal reflux during and shortly after infusion.
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PMID:[Effect of Pitressin (8-arginine vasopressin) on the lower esophageal sphincter in dogs]. 647 51

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

To characterize the influence of extracellular volume status on vasopressin pharmacokinetics, eleven young (aged 19-31 yr) and four old (aged 62-80 yr) subjects received bolus injections of 1 mU/kg Pitressin or synthetic arginine vasopressin following 6 days of sodium depletion (10 meq Na/day) or sodium loading (250 meq Na/day). In six young subjects the rapid decline in plasma vasopressin (pAVP) following the initial peak was interrupted by a second peak 5-30 pg/ml in magnitude 7.5-20 min after injection. In four of these subjects the second peak was larger following sodium depletion as compared with sodium loading. In the elderly a small (4 pg/ml) second peak was present in one sodium-depleted subject. Of five sodium-depleted subjects with central diabetes insipidus, none showed a secondary rise in pAVP. These results indicate that exogenous vasopressin may stimulate the release of endogenous AVP, an effect that appears to be enhanced by sodium depletion and is virtually absent in the elderly. There was no effect of age, volume status, or diabetes insipidus on AVP pharmacokinetics.
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PMID:Effect of exogenous vasopressin on vasopressin release. 669 7

Arginine vasotocin (AVT) has been measured in neonatal cerebrospinal fluid (CSF) and human amniotic fluid using a newly developed specific radioimmunoassay system. There were significant amounts of AVT in all samples. Vasopressin and oxytocin also were measured in the samples and could not account for the levels of vasotocin found. The source and function of these neurohypophyseal peptides in CSF and amniotic fluid remains speculative.
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PMID:Radioimmunoassay of vasotocin, vasopressin, and oxytocin in human neonatal cerebrospinal and amniotic fluid. 669 69


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