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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possible role of microvesicles and vacuoles in the recapture of membrane after pituitary hormone release by exocytosis has been studied in homozygous Brattleboro rats. These mutant animals are unable to synthesize vasopressin and exhibit a steady state hypersecretion of oxytocin from the neural lobe as a result of the osmotic imbalance caused by their diabetes insipidus. This can be converted to a second steady state which approximates to the rate of secretion found in normal Long Evans rats by the administration of exogenous vasopressin daily for 30 days. In the Brattleboro rat, presumptive oxytocinergic nerve endings contain typical 160-170 nm diameter neurosecretory granules; other magnocellular nerve endings contain a population of smaller (approximately 100 nm diameter) dense-cored granules. The number of dense-cored granules was reduced in both types of nerve ending in the hypersecreting Brattleboro rats, but increased as a result of vasopressin treatment to levels which, for the classical neurosecretory granules, approximated that found in Long Evans rats. The microvesicle population of the nerve endings was essentially similar in quantitative terms in all the three groups (i.e. hypersecreting Brattleboro rats; vasopressin-treated Brattleboro rats and Long Evans controls). The number of vacuoles, on the other hand, was increased in nerve endings in the hypersecreting animals but reduced to levels found in Long Evans rats in the Brattleboro animals treated with vasopressin. Furthermore, the size of the vacuoles was comparable to the size of the dense-cored granules contained in the nerve endings. These changes in the vacuole population are exactly those that would be predicted for an organelle responsible for recapture of the granule membrane. We therefore conclude that membrane retrieval after exocytosis of neurosecretory granules in the neural lobe is achieved by vacuoles and that these organelles probably retrieve the membrane of the granule intact.
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PMID:Membrane retrieval by vacuoles after exocytosis in the neural lobe of Brattleboro rats. 712 29

Intracerebroventricularly (i.c.v.) administered angiotensin II (ANG II) at a dose of 100 ng caused a large increase in plasma oxytocin levels in Long Evans (LE) rats and in rats heterozygous for hypothalamic diabetes insipidus (HZ). In rats homozygous for diabetes insipidus (DI) even 100 fold higher doses of ANG II i.c.v. exerted only marginal effects on oxytocin release. The impaired responsiveness in DI rats was fully restored by prolonged treatment with a vasopressin (AVP) analogue. These data show that the decreased sensitivity of ANG II receptors in DI rats is due to the AVP defect and its metabolic consequences and can be reversed by AVP substitution.
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PMID:Angiotensin stimulates oxytocin release: imparied response in rats with genetic hypothalamic diabetes insipidus. 712 94

A new extremely sensitive radioimmunoassay to measure plasma AVP has been developed. Antiserum to AVP of high affinity (Keq = 1.1 X 10(12) 1/mol), raised in rabbits, showed little cross-reaction with related analogues (LVP less than 0.03%, AVT, DDAVP, OXT less than 0.01). The specific activity of 125I-AVP (chloramine T method) was 1400-1750 Ci/mmol. The limit of detection of plasma AVP, after extraction of 2 ml plasma with Florisil, was 0.3 pmol/1. Coefficient of variations of plasma control (2 pmo1/1) were 9.7% (intraassay) and 15.3% (inter-assay), n = 15. Osmotic stimulation by hypertonic saline infusion caused a linear response in plasma AVP in normal subjects, but plasma AVP remained undetectable in patients with cranial diabetes insipidus. Suppression of AVP secretion by a standard oral water load and by alcohol and fluid in volunteers produced low or undetectable values of plasma AVP. In a patient with the syndrome of inappropriate antidiuresis, plasma AVP concentration was grossly elevated.
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PMID:A new sensitive radioimmunoassay for plasma arginine vasopressin. 716 99

A patient is described who developed diabetes insipidus during pregnancy. During a revised Carter test performed at 36 wk gestation using DDAVP (1-desamino-8-D-arginine-vasopressin), uterine activity was recorded with a maximum activity of 120 Montevideo Units. The induction of uterine activity by DDAVP in our patient might be related to the high endogenous oxytocin levels or to the far advanced state of amenorrhea. Post partum, the patient reported decreased vision, and the visual fields were found to be abnormal. A neurosurgical procedure followed, and the diagnosis of craniopharyngioma was made.
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PMID:Diabetes insipidus in pregnancy as a first sign of a craniopharyngioma. 718 32

The Brattleboro diabetes insipidus mutant is incapable of synthesizing vasopressin, but is activated in its production and release of oxytocin. In the homozygous female mutant, there were abnormally short and long oestrous cycles and reduced conception rates after mating with mutant males, a shortened gestation length, and a shorter time-course of labour. A better conception rate when mutant females were mated with normal Brattleboro males indicates the involvement of a male factor in the subfertility. The reduced litter size in diabetes insipidus rats appeared neither dependent of the male's genotype, nor due to a decreased viability of diabetes insipidus fetuses.
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PMID:Reproduction in Brattleboro rats with diabetes insipidus. 720 75

A 23 year old woman with diabetes insipidus who had previously been treated with pitressin, pituitary snuff and chlorpropamide, was treated with DDAVP during pregnancy. DDAVP concentrations immunoassayed as vasopressin were determined in maternal serum and breast milk. Oxytocin antibodies were also determined in maternal serum.
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PMID:DDAVP treatment of diabetes insipidus during pregnancy and the post-partum period. 722 15

Brattleboro rats, homozygous for diabetes insipidus, and Long-Evans rats were anaesthetized with urethane, and antidromically identified neurons were recorded from the supraoptic nucleus. Phasically firing neurones were studied during repeated electrical stimulation of the neural stalk, whereby most supraoptic neurones, but not the recorded neurone, were activated antidromically. Such stimulation consistently modified the discharge pattern of phasic neurones in Long-Evans rats, but was relatively ineffective in Brattleboro rats. These results suggest that the effects of neural stalk stimulation on discharge patterns in Long-Evans rats may be substantially mediated by the evoked release of vasopressin or neurophysin.
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PMID:Effects of neural stalk stimulation on phasic discharge of supraoptic neurones in Brattleboro rats devoid of vasopressin. 726 20

An adolescent boy with essential hypernatremia, absent corpus callosum, mental retardation, hypodipsia, and partial diabetes insipidus with "inappropriate" ADH regulation and secretion was studied regarding factors controlling ADH and neurophysin release. Persistent hyperosmolality was noted while on 100 mEq sodium intake daily. Endogenous vasopressin activity was demonstrated after prolonged water deprivation. Hypertonic saline infusion produced increased volumes but dilute urine. Aqueous pitressin increased urinary osmolality, decreased serum osmolality, urine flow rate, and free water clearance. Stable water diuresis was induced by water loading and on normal saline infusion. Nicotine-stimulated neurophysin remained unexpectedly low and below the level of detectability when sampled during the physiologic studies, whereas oestrogen-stimulated neurophysin was elevated during oestrogen stimulation, water loading, and orthostasis procedures. Plasma vasopressin was suppressed with water loading but remained suppressed 90 min after tilt table testing. These data indicate impairment of the osmoreceptor mechanism: however, since the patient had a normal response of oestrogen-stimulated neurophysin, that part of the neurohypophysis appears intact. Chlorpropamide was effective in alleviating the hyperosmolar state acutely and maintained normal osmolar concentrations during two years of therapy.
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PMID:Essential hypernatraemia, antidiuretic hormone and neurophysin secretion: response to chlorpropamide. 746

Circulating concentrations of oxytocin increase to 10-40 pM in rats in response to osmotic stimuli, suggesting that oxytocin could play a role in regulation of water balance. The present studies tested whether oxytocin at such concentrations increases osmotic water permeability (Pf) in isolated perfused terminal inner medullary collecting ducts (IMCD). In IMCD segments from Sprague-Dawley rats, 20 pM oxytocin added to the peritubular bath caused a two- to threefold increase in Pf, whereas 200 pM oxytocin increased Pf by five- to sixfold (n = 8, P < 0.01). IMCD from Brattleboro rats, which manifest central diabetes insipidus, exhibited a 2.8-fold increase in Pf in response to 20 pM oxytocin and a 4.7-fold increase in response to 200 pM oxytocin. However, in Brattleboro rats, the response to 20 pM oxytocin was dependent on prior water restriction of the rats. Immunoblotting showed no change in the expression of the aquaporin-CD water channel in Brattleboro rats in response to water restriction. Nevertheless, immunofluorescence studies of inner medullary tissue from Brattleboro rats revealed a marked redistribution of the aquaporin-CD water channels to a predominantly apical and subapical localization in IMCD cells in response to water restriction, similar to the redistribution seen in response to vasopressin. Mathematical modeling studies revealed that the measured increase in Pf in response to oxytocin is sufficient to generate a concentrated urine. We conclude that oxytocin can function physiologically as an antidiuretic hormone, mimicking the short-term action of vasopressin on water permeability, albeit with somewhat lower potency.
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PMID:Oxytocin as an antidiuretic hormone. I. Concentration dependence of action. 754 52

The neurohypophysial peptide oxytocin (OT) is released in response to different stressors and has been suggested as a 'stress hormone'. In addition, we have recently shown that centrally administered histamine (HA), which is a mediator of stress-induced release of ACTH and prolactin (PRL), stimulates OT secretion. The aim of the present investigation was to further characterize the HA-induced OT secretion with respect to the type of postsynaptic receptor involved and to investigate the possible role of OT in HA- and stress-induced ACTH and PRL secretion. We studied (1) the effect of HA, HA agonists and HA antagonists on OT secretion in normal male rats, (2) the secretion of OT in response to HA stimulation and to restraint stress, endotoxin stress [lipopolysaccharide (LPS) administration] and insulin/hypoglycemia stress and compared the OT response to that of arginine vasopressin (AVP), (3) the OT response to restraint stress or HA in normal and AVP-deficient Brattleboro rats (DI) suffering from diabetes insipidus and (4) the effect of inhibiting the oxytocinergic system by immunoneutralization or receptor blockade on HA- and stress-induced ACTH and PRL release in normal as well as in DI rats. HA, an H1 and an H2 receptor agonist, stimulated the OT secretion dose-dependently. The HA-induced release of OT was inhibited by pretreatment with an H1 or an H2 receptor antagonist. Restraint stress and HA but not LPS or insulin stress induced an increase in peripheral OT levels, whereas only LPS stress and HA caused an increase in circulating AVP levels. Neither an OT antiserum nor an OT antagonist inhibited the HA- or restraint-stress-induced ACTH or PRL release in normal rats. AVP-deficient DI rats showed, in comparison with their nondeficit counterparts, an increased basal level of OT and no increase in OT levels following restraint stress, whereas the OT response to HA was similar in the two rat types. In AVP-deficient rats immunoneutralization of OT had no inhibitory effect on the HA- and restraint-stress-induced ACTH and PRL response. The ACTH and PRL response to restraint stress and the ACTH response to HA was impaired in DI rats compared to their healthy controls. We conclude (1) that HA stimulates OT secretion via activation of postsynaptic H1 and H2 receptors, and (2) that, in contrast to AVP, OT does not seem to be involved in HA- and restraint-stress-induced ACTH and PRL secretion.
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PMID:Involvement of oxytocin in histamine- and stress-induced ACTH and prolactin secretion. 765 94


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