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)

A sc injection of 2 micrograms arginine vasotocin (AVT) administered every 2 h for a 25-h period starting 1 h after castration of adult male rats caused a 43% reduction (P less than 0.05) in plasma levels of LH compared to diluent-treated castrated controls. In Exp 2, a sc injection of 5 micrograms AVT or diluent was administered to intact or acutely castrated male rats every 3 h for 48 h. After AVT administration, both plasma LH (P less than 0.001) and FSH (P less than 0.05) were significantly reduced, with a concomitant increase in pituitary levels of these gonadotropins. Using the same injection regimen in Exp 3, 250 micrograms melatonin had no effect on plasma or pituitary levels of LH in castrated male rats. In the fourth experiment, neither 1 IU arginine vasopressin nor 1 IU oxytocin had an effect on plasma or pituitary levels of LH, whereas 1 IU of AVT significantly lowered plasma levels of LH (P less than 0.05) and prevented the fall in the pituitary level of this gonadotropin (P less than 0.01) when compared to diluent-treated castrated control rats. Oxytocin (1 IU) significantly inhibited (P less than 0.01) plasma levels of FSH and raised plasma levels of PRL (P less than 0.01) in castrated male rats. No effect on plasma titers of PRL were observed after treatment of castrated rats with AVT in Exp 2 or 4. It is concluded that in acutely castrated male rats, AVT could possibly act either on the hypothalamus and/or the pituitary to affect pituitary and plasma levels of gonadotropins.
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PMID:The effect of subcutaneous injections of melatonin, arginine vasotocin, and related peptides on pituitary and plasma levels of luteinizing hormone, follicle-stimulating hormone, and prolactin in castrated adult male rats. 44 49

By using a specific heterologous double-antibody RIA, changes in the blood levels of PRL during pregnancy, pseudopregnancy, and lactation have been investigated for the first time in the rabbit. Blood levels fluctuate during early and midpregnancy in a manner similar to that in pseudopregnancy. Levels decline in the third trimester of pregnancy and increase dramatically (3- to 25-fold) at or 1--2 days before delivery. Pituitary levels of PRL showed no significant alteration, and fetal serum and amniotic fluid levels of PRL remain low (less than 10 ng/ml) throughout pregnancy. No significant PRL-like, GH-like, or placental lactogen-like activity could be demonstrated either in serum or in extracts of placenta (n = 262) taken between days 10 and 31 of pregnancy. Postpartum blood levels of PRL were similar in lactating and postpartum nonlactating females. In lactating females, suckling evoked an immediate increase (15- to 25-fold) in circulating PRL levels. Handling the female or the iv injection of oxytocin during lactation did not cause PRL release. In contrast, manual test stimulation caused an immediate increase in blood levels of PRL and a response pattern very similar to that of natural suckling. These results suggest that PRL release during suckling occurs solely in response to the tactile stimulation of the teats.
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PMID:Prolactin during pregnancy and lactation in the rabbit. 57 Apr 85

By the 5-day culture of bovine granulosa cells both in serum-free and in serum-supplemented medium the time-dependent accumulation of PRL immunoreactivity was observed. FSH additions (10-10,000 ng/ml medium) led to a dramatic rise of immunoreactive PRL in a dose-dependent manner. LH stimulated the increase of PRL-like substance only in a great dose (10 IU/ml). Lower LH doses (0.01-1 IU/ml) had no significant influence on this process. Low doses of oxytocin (1 or 10 mIU/ml) blocked, and higher ones (100 or 1,000 mIU/ml) stimulated the granulosa PRL-like substance accumulation. Arginine-8-vasopressin (1-1,000 ng/ml), arginine-8-vasotocin (10-10,000 ng/ml), or LH-RH (10-10,000 ng/ml) failed to influence the PRL immunoreactivity accumulation in the culture medium. Present data may suggest the production of PRL-like substance by bovine ovarian cells, as well as the involvement of gonadotropins and oxytocin in the regulation of this process.
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PMID:Prolactin-like substance secretion by granulosa cells isolated from bovine ovaries. 134 Jun 86

Earlier studies have shown that lactation-induced bone loss in the rat is both PTH- and vitamin D-independent and have suggested the involvement of another, as yet unidentified, factor(s) in the altered calcium metabolism which accompanies lactation. In the present study, we investigated the possibility that PTH-related protein (PTHrP), which is produced in lactating mammary glands, is a putative calciotropic factor acting systemically during lactation. To test this hypothesis, we examined changes in urinary phosphate and cAMP excretion in relation to suckling since phosphaturia (P-uria) and increased urinary cAMP excretion are sensitive parameters of PTHrP action on the kidney. When lactating rats (separated from their pups overnight) were allowed to suckle pups for 1 h, they showed a marked P-uria which lasted 3-4 h. In most instances, a transient increase in cAMP excretion preceded the P-uria. These effects were not abolished by thyroparathyroidectomy; hence they are not attributable to a transient increase in PTH secretion. Administration of PRL or oxytocin did not induce significant P-uria. When lactating rats were pretreated with anti-PTHrP anti-serum, the suckling-associated P-uria was prolonged and augmented. This prolongation of P-uria was similar to the effects observed when exogenous PTHrP (1-34)amide was administered in the presence of the antiserum. These data support the hypothesis that some of the PTHrP produced in lactating mammary glands may be released systemically during suckling and act in an endocrine manner on target organs such as the kidney.
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PMID:Suckling-mediated increases in urinary phosphate and 3',5'-cyclic adenosine monophosphate excretion in lactating rats: possible systemic effects of parathyroid hormone-related protein. 165 80

PRL secretion is regulated by an endogenous stimulatory rhythm of PRL-releasing factors within the hypothalamus. The endogenous rhythm has a bimodal periodicity with a nocturnal component which peaks at approximately 0300 h and a diurnal component that peaks at approximately 1700 h. Several PRL-releasing factors are known to be involved in this rhythm. Among these are oxytocin (OT), vasoactive intestinal peptide, and serotonin. We have proposed that OT is the neurohormone that stimulates PRL release from the lactotroph. In this study, we examined the activity of OTergic neurons in the paraventricular nucleus using the expression of the protooncogene c-fos (Fos) as a marker of neuronal activity. Ovariectomized rats were killed at either 0300, 1200, or 1700 h and brains quickly fixed by perfusion with 2.5% acrolein in 4% paraformaldehyde. Brains were blocked and processed for OT/Fos immunohistochemistry. Rats killed at 0300 and 1700 h had significantly greater proportion of Fos expressing OTergic neurons than control rats (1200 h). Percent of Fos-positive OTergic neurons were 2- and 1.5-fold greater at 0300 and 1700 h than 1200 h, respectively. The majority of these neurons were located in the medial parvocellular paraventricular nucleus and periventricular area. In another experiment, groups of OVX rats were killed every 2 h over a 24-h period and OT extracted from their anterior and posterior pituitaries. OT was present in the anterior pituitary in a bimodal rhythm. OT concentrations were greatest at approximately 0400 h and slowly declined to baseline by 1000 h. Another peak of OT was present in the anterior pituitary at approximately 2000 h and quickly declined to baseline by 2400 h. This rhythm of OT was not reflected in either the posterior pituitary or trunk blood. These data suggest that activity of a specific population of OTergic neurons of the paraventricular nucleus is rhythmic. The periodicity of these neurons mirrors that of the endogenous stimulatory rhythm. Furthermore, the anatomical location of these neurons suggests that they may project to the median eminence. Indeed, this heightened activity is reflected in a bimodal rhythm of OT in the anterior pituitary. Taken together, the data presented here provide compelling support for the role of OT as the neurohormone in the mechanism of the endogenous stimulatory rhythm.
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PMID:Activity of oxytocinergic neurons in the paraventricular nucleus mirrors the periodicity of the endogenous stimulatory rhythm regulating prolactin secretion. 172 95

The action of acute administration of oxytocin (OXY), vasopressin (AVP) or its analog 1-deamino-8-D-arginine-vasopressin (dDAVP) on basal and stress induced PRL release in normal male rats and the effect of chronic injection of AVP on PRL stress response in AVP deficient rats were studied. The hormones (OXY, 600 ng min-1 per rat; AVP 6, 12 or 24 ng min-1 per rat and dDAVP 24 ng min-1 per rat) were infused to conscious rats via the jugular vein for 10 min and then the rats were immobilized under continuing the infusion for further 20 min. In parallel experiments arterial blood pressure (BP) was measured. OXY and 24 ng min-1 AVP caused high BP elevation of the same magnitude, yet the effect of 12 ng min-1 AVP was significantly lower. Neither OXY, dDAVP, nor 6 and 12 ng min-1 of AVP affected basal or stress stimulated PRL values when compared with saline treated animals. 24 ng min-1 of AVP highly stimulated nonstressed PRL levels and no additional stress effect was observed. Intramuscular injection of 2 micrograms (1 U) of AVP daily for 7 days did not influence the basal values or stress induced PRL response in Brattleboro homogygous rats as compared with vehicle treated controls or heterozygous rats treated with AVP or vehicle. These results show that the infusion of 24 ng min-1 per rat of AVP stimulated PRL release which cannot be explained by the nonspecific effect of high BP. Repeated AVP administration did not modulate either the basal or IMO stress stimulated PRL secretion in rats with or without genetic vasopressin deficiency.
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PMID:Do the circulating neurohypophysial hormones affect basal or stress induced prolactin (PRL) release in male rats? 176 5

The present study was undertaken in order to establish whether oxytocin (OT) affects the dopaminergic control of PRL secretion in normal women during follicular, periovulatory and luteal phase of their menstrual cycle. For this purpose, 22 normal women were tested with a lower (1 mg) or higher (10 mg) dose of the dopaminergic antagonist metoclopramide (MCP) with or without the concurrent treatment with OT (2 IU injected plus 0.033 IU/min infused for 2 h). Since OT was found unable to modify the effect of either 1 or 10 mg MCP, in additional experiments the same doses of MCP and OT were administered after dopamine (0.04 micrograms/kg/min for 2 h) infusion. Also in these experimental conditions OT failed to modify the PRL response to MCP. These data argue against a role of OT in modulation of the dopaminergic control of PRL secretion in normal women.
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PMID:Oxytocin does not modify the prolactin response to metoclopramide in normal women. 177 42

The present experiments were designed to test whether the previously reported excitatory and inhibitory effects of dopamine (DA) on the secretion of oxytocin (OT) in lactating rats are exerted at different DA receptor subtypes, and to examine whether one or both of these effects might occur at the level of the posterior pituitary. The basal release of OT in nonsuckled, lactating rats was increased after intravenous administration of the D-1 DA agonist SKF 38393, and this effect, as well as the suckling-induced release of OT, was prevented by treatment with the D-1 DA antagonist SCH 23390, suggesting that DA may exert an important stimulatory influence over OT secretion through an action at the D-1 DA receptor subtype. A small stimulation of basal PRL release was also produced by SKF 38393, but blockade of the D-1 DA receptor did not prevent the suckling-induced release of this hormone. Stimulation of the D-2 DA receptor with PPHT had no effect on basal OT release in nonsuckled rats, but this agent, as well as another D-2 DA agonist, bromocriptine, prevented the suckling-induced release of both OT and PRL. The inhibitory effect of D-2 DA receptor stimulation was blocked by the D-2 DA antagonist domperidone, which increased the basal release of both hormones when given alone. These observations confirm previous findings that inhibitory effects of DA on suckling-induced OT release are mediated through activation of the D-2 DA receptor. To test whether either dopaminergic effect occurs at the level of neurosecretory endings in the neurointermediate lobe (NIL), the stalk-NIL was isolated from lactating rats and perifused in vitro. The stalk-NIL junction was electrically stimulated for 4 s, and the effects of selective D-1 DA and D-2 DA agonists and antagonists on the basal and electrically evoked release of OT and vasopressin (VP) was assessed using the two stimulation (S2/S1) paradigm. Electrical stimulation produced marked increases in release of both neural lobe peptides in a Ca(2+)-dependent manner, and the electrically evoked release of OT, but not VP, was enhanced by the opiate antagonist naltrexone (10 microM). Consistent with the in vivo results, SKF-38393 (20 microM) produced a small, but statistically significant, increase in electrically induced OT release, while SCH 23390 (20 microM) was without significant effect. Neither drug affected the basal release of OT or the basal or electrically stimulated release of VP.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Excitatory and inhibitory dopaminergic regulation of oxytocin secretion in the lactating rat: evidence for respective mediation by D-1 and D-2 dopamine receptor subtypes. 183 Dec 47

The synthesis and release of PRL are regulated by a variety of factors that originate in the hypothalamus, peripheral tissues, or posterior pituitary (PP). We recently reported that coculture of anterior pituitary (AP) and PP cells induced an increase in both PRL cell content and the responsiveness of lactotrophs to TRH. The aim of the present study was to determine whether the augmented response to TRH is due to increased lactotroph sensitivity to this particular secretagogue or to enhancement of the releasable pool of PRL. Cells obtained from anterior pituitaries of adult male rats were plated either alone or together with PP cells at the same total density. Cells cultures were maintained in serum-free medium for 4 days and then incubated for 20 min with the designated substances. Angiotensin-II and TRH evoked a significantly larger release of PRL in AP + PP cocultures than in AP cells cultured alone; the greatest difference between the culture types was observed at the highest concentrations of both secretagogues. The stimulation of PRL release by KCl, the calcium ionophore A23187, and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate was higher in the presence of PP cells than in cultures of AP cells alone, although the magnitude of this effect was lower than that seen with PRL secretagogues. The concomitant application of A23187 and 12-O-tetradecanoylphorbol-13-acetate resulted in an increased response in both types of culture and a greater relative effect of PP cells on the evoked PRL release. In contrast to other secretagogues, oxytocin (OT) elicited a smaller response in AP + PP cocultures than in AP cultures. OT was present in significant amounts in medium from cocultures, apparently after being released from the severed neuronal terminals. When AP cultures were pretreated for 4 days with comparable concentrations of OT, the acute OT-evoked PRL release was greatly diminished. These findings suggest that coculture with PP cells increases the releasable pool of PRL in lactotrophs. The stored PRL is accessible for release by secretagogues known to act via the Ca2+ second messenger system, involving both Ca2+/calmodulin and protein kinase-C pathways. The diminished response of cocultures to OT is probably due to desensitization of lactotrophs by the residual amounts of this peptide present in the disrupted nerve endings.
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PMID:Effects of coculture of anterior and posterior pituitary cells on the responsiveness of lactotrophs to different secretagogues. 193 84

We investigated the role of histamine (HA) in the neuroendocrine regulation of PRL secretion in conscious male rats. Blood samples were obtained by decapitation of the animals at 0 min. Intracerebroventricular infusion of HA (34-540 nmol at -15 min) stimulated PRL secretion dose dependently with an ED50 of approximately 135 nmol. Inhibition of neuronal HA synthesis by the specific histidine decarboxylase-inhibitor (S)alpha-fluoro-methylhistidine (alpha FMH; 100 mumol/kg ip at -6 h or 400 mumol/kg ip at -20 h and -6 h) caused a 50% reduction (P less than 0.01) in the PRL response to 5 min of restraint stress. Inhibition of neuronal HA metabolism by the specific histamine-methyltransferase-inhibitor SKF-91488 (400 and 800 nmol icv at -20 min) augmented the restraint stress-induced PRL release 26% and 37%, respectively (P less than 0.05). The two enzyme inhibitors had no or only modest effect on the basal PRL secretion. Pretreatment with a specific antiserum (0.5 ml) to arginine vasopressin (AVP) or an AVP antagonist (25 nmol) administered iv at -20 min inhibited the PRL response to HA (270 nmol icv) 80% and 45%, respectively (P less than 0.01) and inhibited the PRL response to restraint stress 70% (P less than 0.01). In contrast, pretreatment with a specific oxytocin (OT) antagonist (50 nmol) had no effect on the HA- or stress-induced PRL release. The AVP antiserum showed less than 0.0003% cross-reactivity with OT, and radiolabeled OT did not bind to serial dilutions of plasma from rats treated with the AVP antiserum. The AVP antiserum or the AVP antagonist almost prevented the PRL release induced by iv infusion of 800 pmol AVP or a posterior pituitary extract. Infusion of AVP (24-800 pmol iv at -15 min) stimulated PRL secretion dose dependently. However, the dose of AVP (800 pmol) required to induce an increase in plasma PRL similar to that obtained by HA-stimulation, led to a rise in plasma AVP which was approximately 1000-fold higher than that induced by HA, which increased plasma AVP 2-fold. Restraint stress had no effect on the plasma AVP level. We conclude that neuronal HA participates in the mediation of the PRL response to stress and that the stress- and HA-induced release of PRL may involve AVP, whereas an involvement of OT seems unlikely.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mediation of the stress-induced prolactin release by hypothalamic histaminergic neurons and the possible involvement of vasopressin in this response. 198 13


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