Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For measurement of plasma arginine vasopressin (AVP) in children with central diabetes insipidus (DI), a sensitive and specific radioimmunoassay (RIA) for AVP was developed. The anti AVP serum used in this assay bound 50 percent of an purified 125-I-labeled-AVP (125I-AVP) at a final dilution of 5 X 10(4) and its cross reaction with lysine vasopressin, 1-deamino-8-D-arginine vasopressin and oxytocin were 7, 15, and 0%, respectively. Column chromatography of Sephadex G-25 superfine was used for purification of 125I-AVP and four major peaks of radioactivity were observed. The purified 125I-AVP was found in 3rd peak by the highest binding activity with the anti-AVP serum. On the other hand, extraction of AVP from plasma was carried out by the acetone extraction procedure and as little as 1.2 pg per milliliter of AVP in plasma was detected in this RIA. In dehydration state plasma concentration of AVP was 4.5 +/- 1.1 pg/ml (mean +/- SE) in normal seven children (control), 1.5 +/- 0.2 pg/ml in six patients with complete DI and 3.4 +/- 0.6 pg/ml in five patients with partial DI diagnosed with Miller test (complete DI vs partial DI; p less than 0.02, partial DI vs control; no significant). The evaluation of diagnostic value of AVP level measured with RIA in complete DI and partial DI diagnosed with Miller test based on urine osmolality was discussed.
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PMID:[Development of radioimmunoassay for plasma arginine vasopressin and its application to the diagnosis of children with central diabetes insipidus]. 372 1

These experiments were designed to characterize the nature and extent of diabetes insipidus present in a new model of genetic vasopressin (VP) deficiency, the Roman high avoidance rat homozygous for diabetes insipidus (RHA: di/di strain). The new strain was developed from an initial cross between Long-Evans derived Brattleboro (LE:di/di) rats and normal Roman high avoidance (RHA: +/+) rats, and has been bred to be congenic with the parent RHA: +/+ strain. RHA: di/di rats exhibited polydipsia, excreted dilute urine, and exhibited elevated plasma osmolality. RHA: di/di rats shows a similar urinary response to dehydration as LE: di/di rats. VP was undetectable by radioimmunoassay in the serum, brain, and neurohypophysis of RHA: di/di rats. VP-neurophysin containing cells were not observed in the brains of RHA: di/di rats upon immunocytochemical analysis. Thus, the new RHA: di/di strain exhibits essentially the same profile of diabetes insipidus as the LE: di/di rat. The congenic relationship between RHA: di/di and RHA: +/+ rats makes the RHA: di/di rat a useful model under circumstances where genetic variables unrelated to VP deficiency may confound the interpretation of data.
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PMID:Characterization of a new rodent model of diabetes insipidus: the Roman high avoidance rat homozygous for diabetes insipidus. 373 82

Previously it was found that grafts of supraoptic plus paraventricular areas from 19-day-old foetal normal rats survived in the third ventricle of the brain of 4- to 6-day-old, vasopressin-deficient Brattleboro pups, but could not alleviate their polyuria. In the present series, factors important in graft development were analysed. Again using day-19 fetuses as donors, anterohypothalamus grafts as well as grafts placed near a crushed median eminence survived relatively poorly, but showed the presence of vasopressin neurons immunocytochemically one month post-grafting. Homotopic grafting in the supraoptic nucleus, however, even failed to show surviving vasopressin neurons. Graft survival was improved by the use of donor tissue of fetuses younger than day 19. Parvocellular vasopressin cells were frequently seen, organized into clusters resembling the normal suprachiasmatic nucleus. However, magnocellular neurons, as normally seen in supraoptic and paraventricular nuclei, only survived grafting when taken between days 11 and 15 of fetal age. It was concluded that only immature vasopressin neurons survived grafting under the condition employed. Magnocellular neurons had a limited fiber outgrowth into the host brain and median eminence. Most large neurons only stained with non-specific neurophysin antiserum, not with specific vasopressin-associated neurophysin antiserum. Thin fibers of the parvocellular vasopressin neurons provided only occasional and sparse innervation of the host median eminence and lateral septum (one case), but several examples of massive fiber bundles running dorsally from graft into host brain were observed. These fibers terminated in the thalamic periventricular area, a nucleus that is normally innervated by the vasopressin neurons of the suprachiasmatic nucleus. The failure of the grafts to provide adequate vasopressinergic innervation of the host median eminence probably explains why none of the nearly 200 Brattleboro neonates operated upon showed any sign of relief of their diabetes insipidus. It suggests, however, that the present procedures might be useful in restoring central vasopressinergic functions in the developing Brattleboro rat.
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PMID:Vasopressin neuron survival in neonatal Brattleboro rats; critical factors in graft development and innervation of the host brain. 390 Aug 3

Oxytocin (OT) and vasopressin (VP) were measured by radioimmunoassay in hypophysial portal and peripheral blood from male Wistar rats and heterozygous and homozygous Brattleboro rats anaesthetized with urethane. In Wistar rats the concentrations of OT and VP were about 50 times greater than the concentrations in peripheral blood, whether or not the pituitary gland was left in situ during collection, and also considerably greater than the reported concentrations of the peptides in the cerebrospinal fluid. The release of both peptides was increased significantly by a lesion of the supraoptico-hypophysial tract that led to diabetes insipidus, but which left intact the external layer of the median eminence (ME). Concentrations of VP were undetectable in plasma from homozygous Brattleboro rats, but the portal plasma concentrations of VP in heterozygous Brattleboro rats were not significantly lower than in Wistar rats. The concentrations of OT in portal plasma from both types of Brattleboro rat were significantly higher than in Wistar rats. The output of VP and OT into hypophysial portal blood of Wistar rats was not significantly affected by electrical stimulation of the suprachiasmatic, supraoptic or paraventricular nuclei or the ME using two types of stimuli, one of which produced an increase in peripheral plasma concentrations of VP and OT in intact rats and a significant increase in the release of LH-releasing hormone into hypophysial portal blood. The output of VP and OT into portal blood was also not significantly affected by either adrenalectomy with or without injection of dexamethasone or the injection of either the 5-hydroxytryptamine (5-HT) synthesis blocker, parachlorophenylalanine, or the 5-HT uptake blockers, alaproclate or zimelidine. These results show that large amounts of OT as well as VP are released into hypophysial portal blood from fibres of the hypothalamo-neurohypophysial system that terminate in the external layer of the ME. Although distinct from the fibres that terminate in the pars nervosa (PN), the findings in Brattleboro rats show that the VP fibres of the ME system originate in neurones with a genomic mechanism for VP synthesis similar to that of the VP neurones that project to the PN. The lack of effect of adrenalectomy and the administration of 5-HT synthesis and uptake blockers must be interpreted with caution since the results obtained with electrical stimulation suggest that when the pituitary stalk is cut the release of OT and VP into portal blood approaches a maximum and may therefore be difficult to alter by experimental manipulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Oxytocin and vasopressin in rat hypophysial portal blood: experimental studies in normal and Brattleboro rats. 396 10

The antidiuretic activity of oxytocin (OT) was measured in Brattleboro rats with congenital diabetes insipidus. A dose dependent antidiuretic response was found in animals receiving chronic infusions of 0.1 micrograms/h, 1.0 micrograms/h, and 5 micrograms/h of OT. OT infused at the rate of 5 micrograms/h over a 7-day period completely reversed the symptoms of diabetes insipidus. The results support the concept that OT serves as a weak agonist of vasopressin at the level of the kidney and at pharmacological levels exhibits antidiuretic activity.
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PMID:Antidiuretic effects of oxytocin in the Brattleboro rat. 406 2

1. Rat neurohypophysial extracts have been examined by polyacrylamide-gel electrophoresis. 2. Three of the proteins were tentatively identified as neurophysins by their acidic nature and their disappearance after dehydration of the animals. 3. These proteins were radioactive 24h after intracisternal injection of [(35)S]cysteine. 4. Two of the proteins were present in much greater quantities than the third, and these two were present in the gland in the same ratio as the hormones vasopressin and oxytocin. 5. One of these proteins was absent from glands of rats homozygous for diabetes insipidus but present in heterozygous animals. 6. It is suggested that these two proteins are the vasopressin-neurophysin and oxytocin-neurophysin of the rat.
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PMID:Tentative identification of a vasopressin-neurophysin and an oxytocin-neurophysin in the rat. 513 37

Autoantibodies to vasopressin-secreting cells of human hypothalamus were detected by means of indirect immunofluorescence (IFL) in 13 patients with diabetes insipidus (DI). 11 of 30 patients (36 . 7%) with "idiopathic" and 2 of 32 (6 . 3%) with symptomatic DI were positive, and 139 control patients were negative. The specificity of the reaction vasopressin cells was demonstrated with a 4-layer double-fluorochrome IFL test in which the second sandwich consisted of rabbit antivasopressin or anti-oxytocin counterstained with rhodaminated anti-rabbit immunoglobulin. 5 patients had also antibodies to oxytocin-producing cells. The antibodies reacted with cytoplasmic components distinct from the hormone; they were of IgG, IgA, or IgM class or a combination of these classes, and half of them fixed complement. Maximum titres were 1:32, and the antibodies could not be absorbed out by incubation with vasopressin, oxytocin, neurophysin I, or neurophysin II. Some sera stained as yet unidentified small cells in the hypothalamus. This report suggests that autoimmunity extends to the hypothalamus. Vasopressin-cell antibodies may prove to be useful markers for the diagnosis of an autoimmune variant of diabetes insipidus.
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PMID:Autoantibodies to vasopressin cells in idiopathic diabetes insipidus: evidence for an autoimmune variant. 613 21

The paraventricular nucleus of the rat hypothalamus has been shown to project to the medulla and spinal cord. The proportion of oxytocin-neurophysin (OTNP) axons to vasopressin-neurophysin (VPNP) axons in these structures is unknown. A major difficulty in resolving this problem in previous immunocytochemical studies was the lack of a specific antiserum to each rat neurophysin. In this study two approaches have been used: (1) comparison of immunostaining for neurophysin in normal versus homozygous Brattleboro rats with diabetes insipidus (HODI) which lack VPNP, and (2) application of an antiserum to both rat neurophysins absorbed with HODI rat hypothalamic-pituitary extracts which contain only OTNP. The latter would result in an antiserum specific for VPNP. Our results indicate that the axons which constitute the caudal projections from the paraventricular nucleus are predominately oxytocinergic, the vasopressinergic innervation being limited to the nucleus tractus solitarius, the dorsal motor nucleus of vagus, and the substantia gelatinosa. A similar number of reactive fibers were seen in the medulla and spinal cord of normal and HODI rats. No positive perikarya were observed caudal to the hypothalamus. Fibers in the medulla appeared to terminate in the nucleus of the solitary tract and in the dorsal motor nucleus of the vagus nerve. Positive fibers throughout the cord were present in the substantia gelatinosa and in the intermediolateral grey. The possible role(s) of these projections in integrating autonomic functions and afferent information with neuroendocrine regulation is discussed.
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PMID:Magnocellular hypothalamic projections to the lower brain stem and spinal cord of the rat. Immunocytochemical evidence for predominance of the oxytocin-neurophysin system compared to the vasopressin-neurophysin system. 615 67

In diabetes insipidus (DI) rats, electrical stimulation of the posterior pituitary lobes in vitro promotes the release of corticotropin-releasing factor (CRF). The CRF activity is abolished by preincubation of the posterior lobe media with thioglycolate. Oxytocin, which is released concomitantly into the medium (3.2 mIU/lobe/20 min), accounts for the complete CRF effect. Neural lobe extracts from DI and normal rats contain 40-70% more CRF activity than can be explained by their content in vasopressin and/or oxytocin. The discrepancy between released and extracted CRFs suggests that hypothetical CRFs or potentiating factors are not released from nerve endings or have to be present in high concentrations to manifest their effect.
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PMID:Oxytocin: major corticotropin-releasing factor secreted from diabetes insipidus rat posterior pituitary in vitro. 625 96

Brattleboro rats exhibit diabetes insipidus (DI) because of a genetic autosomal recessive defect in the synthesis of vasopressin; oxytocin is synthesized normally. Preliminary work suggests that elevated circulating oxytocin levels may compensate for the absence of vasopressin. To evaluate the consequences of presumed elevations of oxytocin levels, oxytocin binding and tissue responsiveness have been measured in the uterus and epididymal fat cells of homozygous-DI (HoDI) and heterozygous-DI (HeDI) animals and Sprague-Dawley and Long-Evans controls. Surprisingly, whereas membranes from HoDI rat uteri exhibited an 85% reduction in oxytocin binding, the biological response (contraction) to oxytocin was indistinguishable from the uteri of HeDI or Sprague-Dawley animals. The uterine response to carbachol was also normal in HoDI rats. In contrast, in adipocytes from HoDI animals, the biological response to oxytocin (glucose oxidation) was abolished, whereas the binding of oxytocin was normal; insulin-stimulated glucose oxidation was, however, normal. These results indicate that receptor binding, while critical to hormone action, is not the sole determining factor. With oxytocin action, postreceptor mechanisms are most important in determining oxytocin responsiveness.
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PMID:Oxytocin action: lack of correlation between receptor number and tissue responsiveness. 626 73


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