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)

Recent neuroanatomical and behavioral evidence has indicated that vasopressin (VP) increases pain thresholds. In the present study intracerebroventricular (ICV) administration of both arginine VP (AVP: 75-500 ng) and 1-deamino-8-D-arginine vasopressin (DDAVP: 150-500 ng) elevated tail flick latencies. Oxytocin (OXY, ICV), also elevated tail-flick latencies (150-1000 ng); however this increase was accompanied by "barrel-roll" seizure activity. VP analgesia was eliminated by pretreatment with 1-deamino-penicillamine-2(O-methyl)tyrosine-AVP (dPTyr(me)AVP: 500 ng, ICV), a VP antagonist, but not naloxone (1 or 10 micrograms, ICV), suggesting that VP modulates nonciceptive thresholds through its own binding sites. Conversely, pretreatment with naloxone (1 micrograms, ICV) but not dPTyr(me)AVP (1 microgram, ICV) attenuated the analgesic efficacy of systemic morphine (10 mg/kg), further dissociating VP and central opiate analgesic processes. Finally, systemic pretreatment with dexamethasone potentiated VP analgesia. These data support the notion that VP is a specific non-opioid pain inhibitor.
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PMID:Vasopressin analgesia: specificity of action and non-opioid effects. 649 25

The localization of CRF-41 related peptide was studied in the brain and posterior pituitary of the homozygous rats for the inherited diabetes insipidus (Brattleboro strain, DI) and of the Long-Evans rats (LE) as control. It was compared to the distribution of vasopressin (AVP), oxytocin (OXY) and OXY-neurophysin (N I). In both strains, CRF-41 was identified in two morphologically distinct systems: one was a hypothalamoneurohypophysial system simultaneously containing CRF-41, OXY and N I; the other was a hypothalamoinfundibular system carrying CRF-41 only. CRF containing neurons were located in the periventricular area of the anterior hypothalamus, in the retrochiasmatic part of the supraoptic nuclei (SON) and, for some of them, in the antechiasmatic part of SON. CRF immunostainings were enhanced by colchicine treatment in LE rats and by DDAVP therapy in DI rats.
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PMID:Comparative immunocytochemical localization of corticotropin releasing factor (CRF-41) and neurohypophysial peptides in the brain of Brattleboro and Long-Evans rats. 660 39

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

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

The effects of SR 49059, a new non-peptide, selective arginine vasopressin (AVP), V1a antagonist, were investigated both on AVP's receptors and on the mitogenic effects of AVP on Swiss 3T3 fibroblasts. We characterized the AVP V1a receptors on Swiss 3T3 cell membranes using the new highly specific AVP V1a radioiodinated ligand, 125I-linear AVP antagonist. Specific binding of the 125I-linear AVP antagonist was saturable, time-dependent and reversible. A single class of high affinity binding sites was identified with an apparent Kd of 40 +/- 20 pM and a Bmax of 63 +/- 20 fmol/mg protein. 125I-Linear AVP antagonist binding to its receptors was potently inhibited in a concentration-dependent manner by AVP, by the peptide V1a antagonist d(CH2)5Tyr(Me)AVP and by the synthetic V1a antagonist, SR 49059 (IC50 in the nanomolar range) while OPC-21268, another non-peptide compound, was about 100-fold less potent. Both DDAVP, a selective V2 agonist, and oxytocin exhibited low affinity (IC50 > 1 microM) in agreement with the AVP V1a nature of the site identified on Swiss 3T3 cells. In addition, the broad-spectrum antiproliferative agent [Arg6, D-Trp7,9, MePhe8] substance P (6-11), was also able to interact at 3T3 AVP V1a receptors (IC50 = 395 +/- 170 nM). The mitogenic effects of AVP on quiescent Swiss 3T3 cells, assessed through [3H]thymidine incorporation, were selectively, stereospecifically and strongly inhibited by SR 40959 (IC50 = 14 +/- 2 nM) while OPC-21268 was inactive up to 220 nM. SR 49059 was even about six times more efficient than d(CH2)5Tyr(Me)AVP in inhibiting AVP-induced DNA synthesis. Moreover, SR 49059 fully inhibited Swiss 3T3 fibroblast proliferation since it completely blocked AVP-stimulated 3T3 cell growth from the G1/G0 into the S/G2M phase, as evidenced by cell cycle analysis using a cytofluorometer. In summary, SR 49059, through direct interaction at AVP V1a receptors, exerts the most potent antiproliferative effect yet described for any V1a antagonist on Swiss 3T3 cells.
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PMID:Effect of a new, potent, non-peptide V1a vasopressin antagonist, SR 49059, on the binding and the mitogenic activity of vasopressin on Swiss 3T3 cells. 812 42

Recent progress in the diagnosis and treatment of diabetes insipidus (DI) is reviewed. Response of plasma vasopressin (AVP) to 5% hypertonic saline can be a new indicator of the capacity of AVP response to osmotic stimuli. Marked progress in the imaging analysis by computed tomography and magnetic resonance imaging (MRI) has made it possible to evaluate hypothalamic-pituitary lesions in detail. Especially, signal intensity on T1-weighted MR image of neurohypophysis is suggested to reflect its function. Sequencing analysis of genes encoding AVP-neurophysin precursor or AVP receptor is expected to be a most useful method for the diagnosis of inherited DI. Intranasal administration of DDAVP (1-deamino-8-D-AVP) is recommended as a standard therapy for DI.
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PMID:[Recent progress in the diagnosis and treatment of diabetes insipidus]. 825 49

Arginine vasopressin (AVP) has been shown to have a unique sensitization effect whereby repeated injection of AVP into a lateral cerebral ventricle or a mediobasal region of the rat forebrain below the lateral septum and including the anterior hypothalamus referred to as the ventral septal area, causes enhanced motor responses to the ligand. To elucidate possible neuronal mechanisms responsible for AVP sensitization, 1) we determined the dose and the time required for the development and expression of AVP sensitization, and 2) we tested the hypotheses that AVP sensitization may result in a) alteration of septal AVP V1 receptor affinity or number, and/or b) alteration of septal AVP V1 receptor signal transduction (phosphatidylinositol hydrolysis) mechanisms. Our behavioral data show that the magnitude of AVP sensitization varies with dose and time, and the effect is dependent on the time interval between injections, in that an initial intracerebroventricular AVP injection enhances the sensitivity of the animals to the motor effects of similar AVP injections given 6 h to 6 days later but not to injections given hourly or weekly. No changes in septal AVP binding site density and affinity, as measured by [3H]AVP binding to septal synaptic plasma membrane, were found in sensitized animals; [3H]inositol monophosphate stimulation in response to AVP in septal slices, however, was found to be significantly enhanced. This enhanced [3H]inositol monophosphate stimulation appears specific to a V1-type receptor because it was significantly reduced in the presence of the V1 receptor antagonist, d(CH2)5Tyr(Me)AVP, and was not found using oxytocin or the V2 receptor agonist, DDAVP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Arginine vasopressin-induced sensitization in brain: facilitated inositol phosphate production without changes in receptor number. 848 41

We investigated the effect of selective inhibition of magnocellular arginine vasopressin (AVP) and oxytocin neurons on histamine (HA)- and restraint-stress-induced adrenocorticotropin (ACTH) and prolactin (PRL) secretion in conscious male rats. The inhibition of magnocellular neurons was obtained by inducing chronic hypoosmolality via continuous exposure of the rats to the AVP V2 receptor agonist 1-deamino(8-D-arginine)vasopressin (DDAVP) which was released from osmotic pumps implanted subcutaneously. In DDAVP-treated rats, plasma osmolality and sodium concentration were 273 mosm/l and 130 mmol/l, respectively. In control rats, the corresponding values were 291 mosm/l and 139 mmol/l. HA (270 nmol) administered intracerebroventricularly or 5 min of restraint stress stimulated ACTH and PRL secretion 4- to 11-fold in normoosmolar rats. In hypoosmolar rats, the HA-induced ACTH response was inhibited more than 40% whereas the restraint-stress-induced ACTH response was unaffected. Conversely, the PRL response to HA in hypoosmolar rats was unaffected whereas the PRL response to restraint stress was inhibited by 40%. In summary, chronic hypoosmolality inhibits HA-induced ACTH and restraint-stress-induced PRL secretion indicating involvement of magnocellular AVP in these responses.
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PMID:Selective inhibition of magnocellular vasopressin neurons by hypoosmolality: effect on histamine- and stress-induced secretion of adrenocorticotropin and prolactin. 964 15

A patient with the genetic condition neurofibromatosis type I and no known coagulopathy undergoing cesarean delivery, had diffuse uterine and surgical site bleeding that was not correctable by oxytocin, methylergonovine and PGF2 alpha. Despite good uterine tone, hemorrhage continued from the uterus and the surrounding tissues, persisting even after surgical ligation of the uterine arteries. With no change in her condition, which was behaving clinically as a coagulopathy, an infusion of desmopressin acetate (DDAVP) was begun. The patient's bleeding promptly resolved shortly after infusion of this agent. A review of relevant literature suggests that platelet reactivity of patients with neurofibromatosis type 1 is attenuated in some in vitro conditions. Thus, there may be some theoretical basis for using DDAVP in patients with neurofibromatosis type 1 who have bleeding problems with no other known source, such as in the case presented here.
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PMID:Correction of intraoperative coagulopathy in a patient with neurofibromatosis type I with intravenous desmopressin (DDAVP). 1532 97


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