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 neurotransmitter histamine participates in the neuroendocrine regulation of pituitary hormone secretion by an indirect action at a hypothalamic level where histaminergic neurons are abundant. The effect of histamine is caused by activation of postsynaptic H1- or H2-receptors. Histamine stimulates the secretion of ACTH, beta-endorphin (mediated by CRH and AVP), alpha-MSH (mediated by dopamine and peripheral catecholamines), and PRL (mediated by dopamine, serotonin and AVP), and participates in the stress-induced release of these hormones and possibly in the suckling- and estrogen-induced PRL release. The release of GH and TSH is predominantly inhibited by histamine; however, uncertainty exists regarding its role and the hypothalamic factors involved. Histamine increases the secretion of LH in females (mediated by GnRH), and may be involved in the mediation of the estrogen-induced LH surge. AVP and oxytocin are stimulated by histamine, probably by an effect in the supraoptic and paraventricular nuclei of the hypothalamus.
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PMID:The role of histamine in the neuroendocrine regulation of pituitary hormone secretion. 206 91

Several peptidergic PRL-releasing factors (PRFs) have been described; however, none have been proven to be of primary physiological importance in the control of hormone release. Similarly dopamine withdrawal alone cannot completely explain the profiles of PRL secretion observed under a variety of conditions. We describe here the isolation in semipurified form of both a PRF and a PRL-inhibiting factor (PIF) from bovine neurointermediate lobe (NIL) extracts. Acid extracts of bovine NILs stimulated, in a dose-related manner, PRL release from cultured anterior pituitary cells, even after immunoabsorption of endogenous oxytocin from the extract. PIF and PRF activities were semipurified from NIL extracts by Sephadex chromatography and detected by in vitro and in vitro bioassays. The PRF material could be separated from oxytocin by gel sieving and was active in the presence of dopamine in vitro unlike synthetic oxytocin and in cell preparations in which the oxytocin-responsive lactotrophs had been removed by selective cytotoxin cell targeting using an oxytocin-ricin A chain cytotoxic conjugate. The PRF material stimulated PRL secretion in a dose-dependent fashion in conscious male rats after iv injection. The PIF material comigrated on sizing gel chromatography with immunoreactive oxytocin and was active in vitro during dopamine blockade with domperidone and in vivo in the presence of endogenous dopaminergic tone. These data suggest that novel factors present in the NIL might exert physiologically relevant control over lactotroph function and add to the growing literature on the presence of a PRF in the NIL.
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PMID:A nonoxytocinergic prolactin releasing factor and a nondopaminergic prolactin inhibiting factor in bovine neurointermediate lobe extracts: in vitro and in vivo studies. 210 31

Our laboratory has provided substantial evidence for the presence of PRL-releasing factor (PRF) in the posterior pituitary. The objectives of this study were 1) to determine the distribution of PRF activity between the neural and intermediate lobes, and 2) to assess the PRF activity of cultured posterior pituitary cells. Posterior pituitaries from adult male rats were dispersed with trypsin and cultured for 1-7 days. Cultured cells or intact posterior pituitaries were extracted with acid and lyophilized. PRF activity was determined by the ability of reconstituted extracts to increase PRL release from cultured anterior pituitary cells. Upon dissection of the posterior pituitary, PRF activity was primarily present in the intermediate lobe. There was minimal contamination between the two lobes, as indicated by the localization of 90% of the total oxytocin in the neural lobe and 95% of alpha MSH in the intermediate lobe. Extracts from intact posterior pituitaries and posterior pituitary cells cultured for 4 days stimulated PRL secretion in a similar dose-dependent manner. Cultured liver and cerebral cortex cells had very low PRF activity. Both oxytocin and dopamine, two neuronal markers, were reduced to less than 5% of their original values within 1 week of cell culture. There was also a significant reduction in the cell content of alpha MSH. On the other hand, PRF activity was relatively stable during culture. Incubation of posterior pituitary cells for 4 days with either cycloheximide or PRL caused a 55-60% reduction of the PRF activity of the cells. We conclude the following. 1) PRF is localized, almost exclusively, in the intermediate lobe of the pituitary. 2) PRF activity is present within nonneuronal cells, either melanotrophs or a small subpopulation of nonopioid-producing cells. 3) PRF is tissue specific, and its presence in cultured posterior pituitary cells depends at least in part on de novo synthesis. 4) The synthesis and/or release of PRF may be subjected to short loop negative feedback regulation by PRL.
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PMID:Prolactin-releasing factor: cellular origin in the intermediate lobe of the pituitary. 211 57

In female rats the mating stimulus induces a bimodal pattern of PRL secretion. A surge of PRL occurs at approximately 0300 h, called the nocturnal surge (N). Another surge occurs at 1700 h on the same day, called the diurnal surge (D). By lowering dopaminergic tone pharmacologically, we have recently demonstrated the existence of an endogenous rhythm stimulatory to PRL secretion in female rats. The periods of this stimulatory influence coincide with the periods of the N and D surges of PRL that occur in mated rats. In addition, we have shown that the 0300 h component of this endogenous rhythm is regulated by oxytocin (OT) and vasoactive intestinal peptide (VIP), and the 1700 h component is regulated by OT and serotonin (5-HT). In this study, we investigated the roles of OT, VIP, and 5-HT in controlling the N and D surges of PRL in ovariectomized (OVX) rats receiving a physiological dopamine-lowering stimulus, copulomimetic stimulation. Blood samples were obtained the day before the experiments between 1700 and 1900 h to verify that the rats used were having surges of PRL in response to cervical stimulation (CS). The role of OT was studied by infusing the OT antagonist 1-deamino-2-D-Trp4-Val8-Orn-OT (OT-A; 0.5 micrograms/kg.min) beginning at either 0100 or 1500 h and continuing for 5 h on day 2 after the last CS. Serial blood samples were obtained immediately before infusion and 60, 90, 120, 150, 180, 240, and 300 min after the start of infusion. The samples overlapped either the N or D surge of PRL. All rats used in these studies demonstrated D surges of PRL the day before the experiment. Saline infusion had no effect on either the N or D surge of PRL in OVX-CS rats. However, infusion of OT-A completely blocked both the N and D surges of PRL. The role of VIP was studied by infusing the VIP antagonist [4-D-Cl-Phe6-Leu17]VIP (VIP-A; 01 micrograms/kg.min) beginning at either 0100 or 1500 h and continuing for 5 h. VIP-A completely blocked both the N and D surges of PRL. To study the role of 5-HT, rats received an acute treatment with p-chlorophenylalanine (PCPA; 250 mg/kg, sc) at either 0100 or 1500 h, and blood samples were taken as before. PCPA had no effect on the N surge of PRL.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Oxytocin, vasoactive-intestinal peptide, and serotonin regulate the mating-induced surges of prolactin secretion in the rat. 213 24

We have previously reported that in contrast to what has been described in adult lung, 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] has specific binding sites in rat fetal lung at the end of gestation, and it stimulates in vitro the phospholipid biosynthesis and surfactant release from fetal rat type II pneumocytes. In the present study an immunohistochemical technique using a rat monoclonal antibody (9A7 gamma) and binding studies were carried out on fresh lung tissues from fetal and newborn rats during the perinatal period to identify the cell(s) directly responsive to 1,25-(OH)2D3 in fetal lung and to look for a down-regulation of the 1,25-(OH)2D3 receptors in the perinatal period. We also searched for a regulation of 1,25-(OH)2D3 binding to fetal lung by 1,25-(OH)2D3 itself and by factors known to affect lung maturation or be involved in parturition. Our results suggest that 1) fetal type II pneumocytes are target cells for 1,25-(OH)2D3; 2) a physiological down-regulation of the 1,25-(OH)2D3 receptors in rat lung occurs in the perinatal period, starting a few hours before birth and lasting at least up to the fifth day of life; and 3) the capacity of rat fetal lung to bind 1,25-(OH)2D3 can be modulated in vitro by different hormones; a small inhibitory effect is observed with oxytocin (100 microU/ml), while PRL (10(-8) M), T4 (10(-6)-10(-10) M), 1,25-(OH)2D3 (10(-9)-10(-10) M), and, to a lesser extent, dexamethasone (10(-7) M) induce a 2- to 4-fold increase in the number of 1,25-(OH)2D3 receptors without altering the binding affinity of receptor for 1,25-(OH)2D3.
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PMID:1,25-dihydroxyvitamin D3 receptors in rat lung during the perinatal period: regulation and immunohistochemical localization. 216 1

Although the posterior pituitary is known to contain the PRL releasing activity or factor (PRF), its chemical identification has been a matter of dispute. In the present study, we purified PRF in porcine posterior pituitary extracts to chemically determine the primary structure. PRF activity was assessed during purification by the release of immunoreactive PRL from superfused rat pituitary cells. Two hundred seventy porcine posterior pituitaries were boiled, homogenized, and extracted with 2 M acetic acid. The acid extract was precipitated with 67% acetone, and the supernatant was absorbed onto a C18 column. The column was eluted step-wise with 10, 20, 30, 40, 50, and 60% acetonitrile (CH3CN) in 0.1% trifluoroacetic acid (TFA). The greatest PRF activity was recovered in the 30% CH3CN/0.1% TFA fraction and was further purified by ion-exchange chromatography on SP-Sephadex, followed by gel-filtration on Sephadex G-50. The Sephadex G-50 fractions with major PRF activity were finally purified by two cycles of reverse phase HPLC, yielding a single peak of PRF. Amino acid, as well as sequence analyses, indicated that the highly purified PRF was oxytocin. Authentic oxytocin showed the same chromatographic behavior and biological activity as those of the isolated peptide. In another experiment, desalted crude extracts of rat and porcine posterior pituitary tissues were directly chromatographed by reverse phase HPLC, and each fraction was assayed for PRF activity. Only two areas showed PRF activity; the largest activity coeluted with oxytocin and the smaller one co-eluted with vasopressin. The fractions which coeluted with oxytocin also showed oxytocin immunoreactivity, as examined by RIA. The results clearly indicated that the major PRF in these posterior pituitary extracts was oxytocin.
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PMID:Oxytocin is the major prolactin releasing factor in the posterior pituitary. 229 52

Oxytocin (OT) has been shown to play a role in the control of physiological PRL release and has been demonstrated to have a direct effect on the pituitary to stimulate PRL secretion. Administration of OT into the third ventricle, however, lowers PRL levels. This reduction could be mediated by either an inhibition of the release of endogenous OT into the hypohysial portal circulation or via an alteration in the release of some other PRL releasing (PRF) or PRL release-inhibiting (PIF) factor. In order to determine if centrally administered OT lowers PRL levels by increasing secretion of dopamine (DA) into the portal circulation, endogenous dopaminergic tone was blocked by injection of the DA antagonist domperidone (DOM). Subcutaneous administration of DOM resulted in elevated PRL levels which could be further augmented by iv infusion of OT (at 0.01 or 0.1 microgram OT/kg.min) or partially, but significantly, reduced by pretreatment with anti-OT antiserum (0.75 ml) indicating that under conditions of DA blockade, OT (which has little PRF activity during conditions of normal dopaminergic tone) can stimulate PRL secretion by a direct pituitary action. Treatment with DOM did not prevent, however, the reduction in PRL levels produced by central administration of OT (2 micrograms). This suggests that the effect of OT to alter PRL secretion when administered into the third ventricle was not mediated via an increase in DA release into the portal circulation. Furthermore, central administration of the OT antagonist CAV-259 (1-deamino-2-D-Trp-4-Val-8-Orn-OT) after DOM treatment resulted in a significant increase in PRL secretion indicating that endogenous levels of OT within the hypothalamus inhibit PRL secretion through a nondopaminergic mechanism. This stimulatory effect of the OT antagonist was not blocked by pretreatment with anti-OT antiserum (iv) which had been demonstrated previously to reduce the PRL surges in lactating mothers and steroid-primed ovariectomized rats, as well as to block the increase in PRL secretion seen after central administration of vasoactive intestinal peptide (VIP). Thus the central effect of OT to alter PRL secretion was probably not due to a change in the release of OT into the portal circulation. Intravenous administration of a VIP antagonist (D-4-Cl-6-Phe-17-Leu-VIP, previously demonstrated to be capable of reducing the PRL surge seen in lactating mothers) into DOM-treated rats does not alter PRL levels but blocks the ability of central administration of the OT antagonist CAV-259 to increase PRL levels under these conditions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Interactions of dopaminergic and peptidergic factors in the control of prolactin release. 229 69

We have recently reported that the posterior pituitary contains PRL-releasing factor (PRF), a small (less than 5000 mol wt) peptide which induces a rapid, hormone-specific, and concentration-dependent stimulation of PRL secretion. Although the identity of posterior pituitary PRF is yet unknown, it is distinct from known PRL secretagogues. Recently, the vasopressin-associated glycopeptide (VAG), which is concentrated in the posterior pituitary, was suggested as a PRF. To investigate whether VAG functions as a PRF, we used Brattleboro rats, which are deficient in arginine vasopressin (AVP), AVP-associated neurophysin, and VAG. Homozygous (DI) and heterozygous (HZ) lactating Brattleboro rats were used. The water consumption of pregnant DI rats (greater than 300 ml/day) was 6-fold higher than that of HZ rats. To correct their water imbalance, DI rats were implanted with osmotic minipumps containing the vasopressin analog 1-desamino-8-D-arginine vasopressin. On days 7-8 of lactation, pups were separated for 6 h, and blood was collected from the dams via a jugular cannula. Upon introduction of the pups, plasma PRL levels increased 100-fold in both DI and HZ rats and remained elevated for the duration of suckling. The suckling-induced rises in plasma oxytocin in DI and HZ rats were also superimposable. The weight gains of the pups of DI and HZ mothers were similar. PRF activity was determined using perifused anterior pituitary cells. Posterior pituitaries from DI and HZ rats contained equivalent amounts of PRF activity. Moreover, purified rat VAG (1.5 and 6.0 micrograms) failed to stimulate PRL release from pituitary cells. The posterior pituitary content of immunoreactive AVP was 2500-fold higher in HZ rats, but the contents of dopamine and oxytocin were similar. It is concluded that VAG neither mediates the suckling-induced rise of plasma PRL, nor stimulates PRL secretion from perifused anterior pituitary cells. Furthermore, posterior pituitaries from DI and HZ rats contain equivalent amounts of PRF activity. Collectively, these data indicate that VAG is not the posterior pituitary PRF.
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PMID:The vasopressin-associated glycopeptide is not a prolactin-releasing factor: studies with lactating Brattleboro rats. 250 Mar 28

We recently reported that acute pharmacologic depression of dopaminergic tone at different times of day unmasks a sex-specific endogenous stimulatory rhythm regulating PRL secretion. The PRL secretory responses of ovariectomized rats to the dopamine antagonist domperidone (DOM) were higher at 0300 and 1700 h than at 1200 h. These are the times during which surges of PRL appear in mated rats. This experimental paradigm was used to investigate the roles of the putative PRL-releasing factors (PRFs) oxytocin (OT), vasoactive intestinal peptide (VIP), and serotonin (5-HT) in this rhythm. The role of OT was studied by infusion of the OT antagonist 1-deamino-2-D-Trp-4-Val-8-Orn-Oxytocin (OT-A, 0.5 microgram/kg min) for 6 h. Two hours after beginning the OT-A infusion DOM was administered, as a single injection of 200 micrograms/kg iv at either 0300, 1200, or 1700 h. Serial blood samples were collected immediately before and 5, 10, 20, 30, 60, 120, 180, and 240 min after DOM administration. Infusion of OT-A attenuated the heightened PRL secretory responses to DOM given at both 0300 and 1700 h but did not affect the response at 1200 h. The role of VIP was studied by infusing the VIP antagonist [D, 4-Cl-Phe6,Leu17] VIP (VIP-A, 0.1 microgram/kg.min) as described above. VIP-A infusion had no effect on the PRL secretory responses to DOM given at 1200 or 1700 h but attenuated the heightened response at 0300 h. In order to study the role of 5-HT in the rhythm, rats were pretreated with p-chlorophenylalanine (250 mg/kg sc) 48 and again 24 h before the experiment. Pretreatment with p-chlorophenylalanine had no effect on the PRL secretory responses to DOM given at 0300 or 1200 h, but it attenuated the augmented PRL secretory response at 1700 h. These data suggest that both VIP and OT act as endogenous PRFs at 0300 h and 5-HT and OT act as PRFs at 1700 h. We propose that VIP and 5-HT are continuously active oscillatory neurotransmitters regulating OT release into pituitary portal blood and that these daily events only eventuate in PRL release when the mating stimulus has release the lactotroph from the inhibitory effects of dopamine.
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PMID:Hypothalamic factors involved in the endogenous stimulatory rhythm regulating prolactin secretion. 252 68

The posterior pituitary contains a PRL-releasing factor (PRF), a small (less than 5000 mol wt) peptide which is distinct from known PRL secretagogues. The objectives of this study were to determine if posterior pituitary extracts specifically stimulate PRL release in vivo and to assess the relative contributions of oxytocin (OT), arginine vasopressin (AVP), and beta-endorphin (beta END) to the PRF activity of the extract. Rat posterior pituitaries or cerebellar tissue were extracted with 1.0 N acetic acid, boiled, and ultrafiltered through 5000 mol wt cutoff membranes. The eluates were treated with performic acid (which oxidizes disulfide bonds and methionine residues), lyophilized, and reconstituted in saline. Jugular blood was collected from conscious ovariectomized rats before and after intracarotid injection of test substances and was analyzed for PRL, LH, and GH by RIA. Injection of 0.3, 1.0, and 3.0, posterior pituitary equivalents increased plasma PRL levels by 2-, 8-, and 22-fold, respectively. PRL levels peaked within 5 min after the injection and returned to basal levels by 30 min. Plasma LH levels decreased slightly, and GH was unchanged. Cerebellar extracts did not affect plasma hormone levels. Injection of OT induced a 4-fold rise in plasma PRL levels. Oxidation of OT was well as AVP with performic acid abolished any PRL-releasing activity. Injection of beta END increased plasma PRL levels by 7-fold. Treatment of beta END with performic acid caused a 60% loss in its ability to release PRL. Pretreatment of rats with naloxone abolished the PRL-releasing effect of beta END, but did not alter the PRF activity of posterior pituitary extracts. We conclude that posterior pituitary extracts stimulate PRL release in vivo in the presence of an intact dopaminergic inhibition. This stimulation is rapid, dose dependent, and hormone specific. OT, AVP, and beta END do not contribute significantly to the PRF activity in the posterior pituitary extract.
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PMID:The posterior pituitary contains a potent prolactin-releasing factor: in vivo studies. 252 28


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