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)

Jugular administration of 200 micrograms PGI-2 salt significantly reduced spontaneous uterine activity in ovariectomized, oestrogen-primed goats; the effect was acute and persisted for about 3 h. Peripheral plasma concentrations of 6-keto-PGF-1 alpha, the stable metabolite of PGI-2, decreased to 50% of initial values after 30 min; but at the start of uterine recovery were in excess of 2 ng.ml-1. Uterine reactivity to both oxytocin and PGF-2 alpha after PGI-2 administration was unaffected.
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PMID:Effect of PGI-2 on uterine activity in vivo in non-pregnant ovariectomized goats (Capra hircus). 251 31

The molecular mechanisms which regulate expression of vasopressin (AVP)- and oxytocin (OT)-encoding genes are unknown. We have investigated the regulatory role of one class of second messenger, the cyclic nucleotides, by examining levels of both adenosine 3',5'-monophosphate (cAMP) and guanosine 3',5'-monophosphate (cGMP) in hypothalamic nuclei of rats during osmotic stimulation. In vivo studies, in which rats were given 2% saline to drink for different periods (salt loading), demonstrated elevated levels of cAMP in the supraoptic nucleus (SON) after 2 days. Raised levels were also evident at 3 and 7 days. A similar (less marked) pattern was observed in the paraventricular nucleus (PVN) but not in the suprachiasmatic nucleus (SCN). cGMP was present at much lower levels than cAMP and did not exhibit parallel dynamics during salt loading; however, significant changes in cGMP levels were found in the SON and PVN. In vitro studies, in which explant cultures of punched hypothalamic nuclei were challenged with hypertonic media, demonstrated that increasing medium osmolality from 290 to 310 mOsm/kg doubled the level of cAMP in the SON but did not change levels in the PVN or SCN. A greater stimulus, 325 mOsm/kg, caused a 4-fold increase in SON cAMP, and small cAMP responses in the PVN and SCN. Marked cGMP responses were also observed in the SON following stimulation at 310 and 325 mOsm/kg, smaller responses being found in the PVN and SCN. These results are consistent with previous demonstrations of SON neuron osmosensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclic nucleotide dynamics in the rat hypothalamus during osmotic stimulation: in vivo and in vitro studies. 254 82

Retrograde tracing was combined with in situ hybridization to demonstrate that a small percentage of neurons of the paraventricular hypothalamic nuclei (PVN) which project to the spinal cord or the medullary vagal complex contain the mRNA to produce the peptides vasopressin or oxytocin. These projection neurons respond to salt loading with an upregulation of mRNA for these peptides. The present study provides an anatomical basis for a direct regulatory influence of PVN neurons on preganglionic neurons in the spinal cord and medulla.
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PMID:Mediation of changes in paraventricular vasopressin and oxytocin mRNA content to the medullary vagal complex and spinal cord of the rat. 261 Sep 47

Carboxypeptidase H (CPH) is a peptide-processing enzyme thought to be involved in the synthesis of many neuropeptides, including vasopressin (VP) and oxytocin (OT). In this study, employing in situ hybridization histochemistry, we have shown that CPH mRNA is abundantly expressed in the magnocellular paraventricular and supraoptic nuclei of the hypothalamus, the primary sites of OT and VP synthesis. Since this enzyme is copackaged in secretory vesicles and hence coreleased with the neurohypophysial hormones, enzyme stores are depleted in parallel with the peptide hormones during states of hypersecretion. Chronic osmotic stimulation, such as occurs in long-term salt-loading or in diabetes insipidus in the Brattleboro rat, causes depletion of neurohypophysial hormone stores and is accompanied by increased rates of neurohypophysial hormone transcription and translation. This study has shown that the expression of CPH mRNA is also significantly increased in oxytocin and vasopressin producing magnocellular neurons during chronic osmotic stimulation of the hypothalamic-neurohypophysial system. CPH mRNA levels in other peptidergic areas of the brain are not significantly changed by osmotic stimulation. These findings illustrate a coordinate regulation of the transcription of peptide hormones and an enzyme required for the hormones' posttranslational processing.
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PMID:Regulation of carboxypeptidase H gene expression in magnocellular neurons: response to osmotic stimulation. 262 43

A combination of autoradiographical techniques and computerized image analysis has been used to study the distribution and density of cholecystokinin receptors in the paraventricular and supraoptic nuclei of animals in which the magnocellular-posterior pituitary axis is activated, namely, in salt-loaded (2% sodium chloride) and homozygous Brattleboro rats. [125I]cholecystokinin octapeptide binding was greatly elevated in the paraventricular, supraoptic and accessory nuclei of salt-loaded and homozygous Brattleboro rats, compared to the respective control animals. Furthermore, under these conditions [125I]cholecystokinin octapeptide binding in the paraventricular nucleus was localized almost exclusively to magnocellular subdivisions, and especially to those containing predominantly oxytocin neurons. Autoradiographical competition studies revealed that the increase in [125I]cholecystokinin octapeptide binding in magnocellular nuclei reflected an increase in receptor number (Bmax) rather than affinity (Kd). These results suggest that cholecystokinin receptor density in the paraventricular, supraoptic and accessory magnocellular nuclei is closely linked to magnocellular neurosecretory activity and raises the possibility that cholecystokinin receptors may be involved in oxytocin and vasopressin release processes.
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PMID:Modulation of hypothalamic cholecystokinin receptor density with changes in magnocellular activity: a quantitative autoradiographic study. 272 63

The hypothalamus is one of the most studied areas of the central nervous system. Many of its functions are understood and there is an extensive literature on its role in the control of pituitary hormone secretion, autonomic nervous system activity, regulation of salt, water and food ingestion, body temperature regulation and aspects of behaviour. Although the role of the hypothalamus in the control of pituitary secretion was postulated in the early 1900s, the chemical nature of these control mechanisms has only been documented in the last few years. The opioid peptides represent one particular family of chemical compounds which have been shown to have many effects on pituitary hormone secretion. Exogenous opioids inhibit the neurosecretion of both vasopressin and oxytocin from the posterior pituitary neurosecretory terminals of hypothalamic cell bodies. Opioids also have major actions on the secretory activity of the anterior pituitary which has no innervation from the hypothalamus, but which is regulated by blood-borne factors in the hypophyseal portal circulation which runs from the median eminence of the hypothalamus. It was therefore of considerable interest when it was discovered that endogenous opioid peptides could be detected both in the neurohypophyseal system and in cells which project into the median eminence. The simple presence of a peptide in a neurone does not necessarily imply a function. If, however, we can demonstrate that regulation of the synthesis of the peptide occurs in a manner which corresponds with the expected role of the agent, this provides powerful data in support of a genuine physiological function. The elucidation of the genomic structure of the precursors for the three endogenous opioid peptides has provided us with the ability to measure mRNA for these peptides in defined areas of the brain and to assess their response to appropriate stimuli. Not only does mRNA for the endogenous opioid dynorphin coexist in the same cells as vasopressin but we have now been able to demonstrate that stimuli to vasopressin secretion also result in a markedly increased accumulation of dynorphin mRNA. Similarly, previous studies have shown that opioid peptides derived from another precursor--pro-enkephalin A--coexist with corticotrophin releasing factor in a different group of hypothalamic cells. We have now been able to demonstrate that stresses which result in an accumulation of corticotrophin releasing factor mRNA also result in increased pro-enkephalin mRNA in the same area. This considerably strengthens the hypothesis that endogenous opioids do play a significant role in the control of hypophyseal secretion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The neuroendocrine paraventricular hypothalamus: receptors, signal transduction, mRNA and neurosecretion. 285 Mar 37

Specific radioimmunoassays were used to measure the effects of hypertonic saline (salt loading), water deprivation, and trichothecene mycotoxin (T2 toxin) on the content of methionine enkephalin (ME), leucine enkephalin (LE), alpha-neoendorphin, dynorphin A, dynorphin B, vasopressin, and oxytocin in the rat posterior pituitary. Concentrations of vasopressin and oxytocin decreased in response to both osmotic stimuli and treatment with T2 toxin, but the decrease was greater with osmotic stimulations. Similarly, concentrations of LE and dynorphin-related peptides declined after salt loading and water deprivation; LE concentrations also decreased after treatment with T2 toxin. The concentration of ME decreased after water deprivation, did not change after salt loading, and increased after T2 toxin treatment. The differentiating effects of these stimuli on the content of immunoreactive LE and ME are consistent with the hypothesis that LE and ME may be localized in separate populations of nerve endings with different roles in the posterior pituitary.
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PMID:Methionine and leucine enkephalin in rat neurohypophysis: different responses to osmotic stimuli and T2 toxin. 285 18

1. Cryostat sections were cut through the hypothalamus of rats which had been given a 2% (w/v) NaCl solution to drink for up to 12 days. 2. In situ hybridization histochemistry was performed on these sections using synthetic oligonucleotide probes against part of the precursor sequence for vasopressin, oxytocin, dynorphin, enkephalin and corticotrophin-releasing factor (CRF). 3. Drinking 2% NaCl solution resulted in a progressive increase of vasopressin, oxytocin and dynorphin mRNAs hybridized in the magnocellular neurones of the supraoptic (s.o.) and paraventricular (p.v.) nuclei. No enkephalin mRNA was detected in the magnocellular areas of the control animals although small quantities of probe did hybridize after 12 days of salt loading and after the stress of I.P. hypertonic saline. 4. Ten-day-lactating female rats were also studied. They had a very marked increase in oxytocin mRNA with smaller increases of vasopressin and dynorphin mRNAs. No detectable enkephalin mRNA was hybridized in the magnocellular s.o. or p.v. nuclei and CRF mRNA was unchanged in both the s.o. nucleus and the p.v. nucleus.
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PMID:Vasopressin, oxytocin, dynorphin, enkephalin and corticotrophin-releasing factor mRNA stimulation in the rat. 289 79

A paradigm was developed for the chronic osmotic stimulation of homozygous diabetes insipidus rats of the Brattleboro strain, a strain that fails to synthesize vasopressin. This study examines the adaptation of 2 sets of coexisting peptide hormone magnocellular neurons in the hypothalamoneurohypophyseal system (HNS) of Long Evans (LE), Brattleboro heterozygote (HZ), and Brattleboro homozygote (DI) rats: (1) the arginine8-vasopressin (AVP)/dynorphin (DYN) neurons, and (2) the oxytocin (OT)/cholecystokinin (CCK8) neurons of the paraventricular and supraoptic nuclei, which project to the posterior pituitary. The regimen of chronic intermittent salt-loading (CISL) involved the replacement of 2% saline for normal drinking water for 18 hr/d. This protocol effectively increased plasma levels of AVP and OT in LE and HZ rats, oxytocin in DI rats, and maintained the posterior pituitary in a state depleted of AVP, OT, CCK, and peptides derived from pro-dynorphin: DYN A 1-17, DYN A 1-8, and DYN B 1-13. The ratio of pituitary DYN A 1-17 to DYN A 1-8 content in DI rats or in LE, HZ, and DI rats following 6 d of CISL suggests a preferential release of DYN A 1-17 during periods of chronic secretory activity. In response to chronic secretory activity, mRNAs for AVP, OT, DYN, and CCK increased 1.5-2-fold in all 3 AVP rat strains, with mRNAs for coexisting peptide hormones displaying parallel increases. Mutant AVP mRNA in the DI rat was expressed at very low levels and DYN mRNA in very high levels, with each of these mRNAs continuing to be regulated by CISL in a normal manner. These results suggest a regulatory relationship between AVP and OT neurons, in which vasopressin neurons are feedback-regulated by AVP, most likely via plasma osmolarity, and that oxytocin neurons are modulated by peptides derived from pro-dynorphin.
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PMID:Regulation of hypothalamic magnocellular neuropeptides and their mRNAs in the Brattleboro rat: coordinate responses to further osmotic challenge. 290 13

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


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