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)

The ability of synthetic atrial natriuretic factor (ANF) to inhibit vasopressin (AVP) release, as well as its action to inhibit water intake and salt preference in the rat, suggest a role for the peptide in the hypothalamic control of fluid volume in addition to its established actions in the kidney. We report here evidence for a direct, hypothalamic site of action of ANF to inhibit, specifically, AVP secretion. Third cerebroventricular infusion of 1.0 (p less than 0.05) and 2.0 (p less than 0.025) nmoles ANF significantly inhibited AVP release in euvolemic, normally hydrated rats while IV doses of ANF failed to significantly alter AVP release except when 5 nmoles (p less than 0.05) were infused. No significant effects on oxytocin (OT) release were observed. Vasopressin release from median eminence or pituitary, neural lobe explants during static, in vitro incubations was not significantly altered by doses of ANF ranging from 10(-12) to 10(-7) molar. Release of AVP during perifusion of neural lobe explants in the presence of ANF was similarly unaffected. However, AVP and not OT release from hypothalamo-neurohypophysial system explants was significantly inhibited in the presence of 10(-8) and 10(-7) M ANF, suggesting an action of the peptide at the levels of the AVP-producing cell bodies in the included supraoptic nucleus either directly or via an action on an interneuron, and not at the AVP-containing terminal fields in the median eminence or neural lobe.
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PMID:Hypothalamic action of atrial natriuretic factor to inhibit vasopressin secretion. 295 84

The hypothalamic paraventricular and supraoptic nuclei and the neurohypophysis of rats were investigated 8 weeks after streptozotocin (STZ)-induction of type 1 diabetes. Vasopressin (VP)- and oxytocin (OT)-containing neuronal profiles were examined using the pre-embedding peroxidase-antiperoxidase technique for electron microscopy. Ultrastructural alterations were observed in the somata, dendrites and axons of VP- and OT-labelled profiles. There was no evidence, however, for alterations in the synapses associated with VP- or OT-labelled somata, dendrites and axons. The results indicate that both VP- and OT-containing neuronal profiles are involved in the ultrastructural reorganisation of the hypothalamo-neurohypophysial complex during diabetic conditions. Depletion of VP- and OT-containing axon profiles in the neurohypophysis may suggest increased release of both neurohypophysial hormones in STZ-induced diabetes.
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PMID:The hypothalamo-neurohypophysial system in streptozotocin-diabetic rats: ultrastructural and immunocytochemical evidence for alterations of oxytocin- and vasopressin-containing neuronal profiles. 296 36

Experiments were designed to study the effects of oxytocin on canine basilar and femoral arteries and to compare these with the effects of vasopressin. Rings of the arteries were suspended in physiological salt solution for isometric tension recording. Oxytocin and vasopressin caused endothelium-dependent relaxation of basilar arteries contracted with prostaglandin F2 alpha. Vasopressin was more potent than oxytocin. In the femoral artery, the two hormones caused endothelium-independent contractions with the same order of potency. The relaxations of the basilar artery occurred at lower concentrations of each substance than the contractions of the femoral artery. The relaxations in response to both agonists were inhibited competitively, and the contractions noncompetitively, by the V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP; the antagonist did not affect endothelium-dependent relaxations in response to bradykinin. Thus, both oxytocin and vasopressin cause endothelium-dependent relaxation of the basilar artery by activating V1-vasopressinergic receptors; the contractions of femoral arteries that they cause also may be mediated in part by V1-vasopressinergic receptors.
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PMID:Oxytocin causes endothelium-dependent relaxations of canine basilar arteries by activating V1-vasopressinergic receptors. 300 Dec 82

Binding of radioactive vasopressin--but not of oxytocin--was detected by autoradiography and by labeling of membranes obtained from the rat superior cervical ganglion. In both instances binding could be displaced by V1 (smooth muscle-type) but not by V2 (kidney-type) agonists, indicating that the ganglionic vasopressin receptors are similar to those present on hepatocytes and vascular smooth muscle. In accordance with the V1 character of the receptors, vasopressin activated the turnover of membrane inositol lipids, and this effect was abolished by a structural analogue known to act as a vasopressor antagonist. A possible physiological role of vasopressin was suggested by intracellular recordings obtained from ganglion cells in vitro. Vasopressin induced a reduction in the amplitude of the fast excitatory postsynaptic potential evoked by electrical stimulation of the preganglionic nerve. This reduction in ganglionic transmission was antagonized by the same synthetic structural analogue that blocked the effect of vasopressin on inositol lipids. This study provides evidence for the presence of functional vasopressin receptors in a rat sympathetic ganglion and thus suggests that vasopressin may play a role in peripheral autonomic function.
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PMID:Biochemical and electrophysiological evidence of functional vasopressin receptors in the rat superior cervical ganglion. 301 44

The hormones of the neurohypophysis, vasopressin and oxytocin, have now been shown to be synthesized as part of a prohormone complex that includes a vasopressin-neurophysin and oxytocin-neurophysin, respectively. In addition, for vasopressin, there is a glycopeptide as part of the prohormone. For each hormone the prohormone is packaged into neurosecretory granules and transported via axons to the posterior pituitary gland. In addition to this "classic" system, axons containing neurohypophyseal hormones project to the median eminence for release into portal vessels, and to other areas of the brain and spinal cord where the peptides may function as neurotransmitters rather than as hormones. As neurotransmitters, the neurohypophyseal hormones may be involved in the regulation of certain autonomic functions. Vasopressin and oxytocin are secreted into the cerebrospinal fluid where there is a diurnal rhythmic secretion of the peptides in several animal species (some species have a predominant rhythm of vasopressin and others a rhythm of oxytocin). Neurohypophyseal peptides are synthesized in some non-neuronal tissues where the function is unknown, and recently a novel peptide with similarities to oxytocin and vasotocin has been identified. The relationship of this novel peptide to the neurohypophyseal peptides is unknown. These new developments are likely to elucidate many new functions for the hormones of the neurohypophysis.
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PMID:The neurohypophysis: recent developments. 302 55

Vasopressin and oxytocin administered subcutaneously and intravenously in a dose of 0.5 IU/kg were studied in experiments on albino male rats for their effect on the glycogen content and gluconeogenesis enzymes activity in the liver as well as on the glycemia level. Neurohormones injected subcutaneously have no effect on the values of the measured indices. Vasopressin already the first 15-60 min after its intravenous injection in the mentioned dose leads to an essential decrease of the glucose content in blood, glycogen amount, glucose-6-phosphatase and fructose-1.6-diphosphatase (EC 3.1.3.9 and 3.1.3.11) activity in the liver of test animals. The intravenous injection of oxytocin in the same dose induces changes in the carbohydrate metabolism indices similar in their direction and magnitude to the effects of intravenous injection of vasopressin.
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PMID:[The role of vasopressin and oxytocin in the regulation of glycemia levels and carbohydrate metabolism in the liver]. 303 60

(1) Oxytocin is synthesized in the luteal cells of all species so far studied, including the human. Vasopressin is also synthesized, but at a much lower rate. (2) The oxytocin-neurophysin gene is expressed in granulosa cells and granulosa-derived luteal cells but not in theca cells. Ovulation or spontaneous luteinization initiates the gene expression which peaks in the early luteal phase and ceases around mid-cycle. (3) Luteal oxytocin concentrations rise with considerable delay after the peak of specific mRNA and reach maximal levels around mid-cycle. Oxytocin concentrations fall to low levels in the late luteal phase and in pregnancy. (4) Thecal tissue produces substances such as catecholamines and ascorbic acid that stimulate oxytocin secretion in granulosa cells. The adrenergic innervation of thecal tissue provides a source of catecholamines and may therefore serve a modulatory function in ovarian oxytocin secretion. (5) Oxytocin has little or no direct effect on luteal progesterone production. (6) Oxytocin inhibits LH-stimulated prostacyclin production in luteal cells of cows. Oxytocin may induce the release of PGF-2 alpha or lipo-oxygenase products from the ovary but this has not yet been documented. (7) PGF-2 alpha releases oxytocin from the ovary but does not turn off its synthesis. (8) The concept that ovarian oxytocin participates in the luteolytic process is gaining acceptance. In some species (sheep, goat) ovarian oxytocin acts as a hormone causing PGF-2 alpha release from the uterus. In others it acts in a paracrine or autocrine fashion on ovarian prostanoid production (cow, possibly primates).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxytocin and ovarian function. 305 1

Vasopressin, vasopressin analogs, forskolin and 8-bromo-cyclic AMP (8Br-cAMP) were studied for their effects on transepithelial water flux in toad urinary bladder. Arginine vasopressin, arginine vasotocin, oxytocin, desamino-8-D arginine vasopressin, forskolin and 8Br-cAMP stimulated hydro-osmotic water flux in a dose-dependent fashion. The rank order of potency was arginine vasotocin greater than arginine vasopressin greater than oxytocin greater than desamino-8-D-arginine vasopressin greater than forskolin greater than 8Br-cAMP. The vasopressin analogs [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-(O-methyl)tyrosine,8-arginine]vasopressin (SK&F 100273), [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-(O-methyl)tyrosine,4-valine,8-arginine]vasopressin (SK&F 100501), [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-D-tyrosine,4-valine,8-arginine]vasopressin (SK&F 100885), [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-(O-ethyl)tyrosine,4-valine,8-arginine]vasopressin (SK&F 100398), [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-D-isoleucine,4-valine,8-arginine]vasopressin (SK&F 101485), [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-(O-ethyl)-tyrosine,4-valine,8-arginine]vasopressin (SK&F 101498), [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid),2-(O-ethyl)D-tyrosine,4-valine,8-arginine,9-desglycine]vasop ressin (SK&F 101926) and [1-(beta-mercapto-beta-beta-cyclopentamethylene propionic acid),2-D-phenylalanine,4-valine,8-arginine] vasopressin (SK&F 101071) antagonized arginine vasopressin-stimulated water flux and displaced the agonist dose-response relationship to the right in a parallel fashion. The most potent antagonists were those having the (O-ethyl)-D-tyrosine substitution at position 2. None of the antagonists tested had any effect on 8Br-cAMP-stimulated water flux at concentrations up to 10(-6)M.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of action and structural requirements of vasopressin analog inhibition of transepithelial water flux in toad urinary bladder. 309 Feb 34

Vasopressin, MSEL-neurophysin and copeptin have been isolated from guinea pig and rat neurophypophyses and their amino acid sequences have been determined. Whereas in rat processing of the three-domain precursor is complete, in the guinea pig a 132-residue fragment including MSEL-neurophysin and copeptin linked by an arginine residue has been characterized. This incomplete maturation (20% of the precursor) could be due to a deletion of an acidic residue in guinea pig copeptin when compared with other mammalian copeptins.
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PMID:[Difference in the maturation of the three-domain vasopressin precursor in the guinea-pig and rat: identification of a neurophysin-copeptin fragment in the guinea pig]. 309 90

Behavioral changes after administration of the neurohypophyseal hormones vasopressin and oxytocin can be observed in animal and man. Several groups attempted to specify these changes in terms of memory or attention processing enhancement for vasopressin and amnesic properties for oxytocin. These interpretations, however, were targets for recent criticism. In a double-blind between-subject comparison with male volunteers receiving arginine-vasopressin (AVP), oxytocin or placebo intranasally prior to the experimental session, we tried to develop an alternative hypothesis on the basis of behavioral and EEG measures. At the beginning of the session subjects had to learn a list of 25 unrelated nouns within five trials. Recall was assessed 1 h later. Neither learning nor long-term recall were affected by peptide treatments. In a second vigilance task subjects had to covertly count eight series of tone pips. Averaged auditory evoked potentials to these tones showed the expected habituation during the course of the task within all three groups. Vasopressin-treated subjects, however, displayed significantly higher amplitudes of the vertex potential as compared to the other treatment groups. AVP effects were most prominent with the longest interstimulus interval. No influences on heart rate or blood pressure were found. Results indicate that vasopressin induces an enhancement of stimulus-related phasic cortical arousal, and that in this respect oxytocin has no effect.
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PMID:Vasopressin but not oxytocin enhances cortical arousal: an integrative hypothesis on behavioral effects of neurohypophyseal hormones. 313 94


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