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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of oxytocin on the ACTH, cortisol, GH and PRL response to physical exercise was investigated in 6 normal men. In addition, the possible involvement of endogenous opioids in the mediation of oxytocin action was evaluated. After fasting overnight, each subject was tested on four mornings at least 1 week apart. Exercise was performed on a bicycle ergometer. The workload was gradually increased at 3-min intervals until exhaustion and lasted about 20 min in all subjects. Tests were carried out under administration of oxytocin (2000 mIU as an iv bolus injection plus 32 mIU/min per 30 min) or naloxone (10 mg as an iv bolus injection) alone; furthermore, the effect of oxytocin together with naloxone (10 mg as an iv bolus injection) was evaluated. In the remaining test, normal saline was given instead of drugs. Plasma ACTH, cortisol, PRL and GH concentrations were significantly increased by physical exercise. Administration of oxytocin, naloxone or their combination was without effect on the PRL and GH rise elicited by exercise. In contrast, the exercise-induced ACTH and cortisol response was significantly raised by naloxone and reduced by oxytocin. When oxytocin was preceded by administration of naloxone, the ACTH and cortisol response to exercise was not reduced by oxytocin. These data show that oxytocin is capable of inhibiting the rise in ACTH and cortisol, but not in GH and PRL induced by physical exercise. Since naloxone abolished the inhibitory effect of oxytocin, oxytocin action on ACTH and cortisol secretion might be supposed to be mediated by an opioid pathway.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxytocin reduces exercise-induced ACTH and cortisol rise in man. 284 72

The ability of centrally administered vasoactive intestinal peptide (VIP) to stimulate PRL secretion when injected intracerebroventricularly could be due to leakage to the pituitary, where it is known to exert direct PRL-releasing activity, or to a hypothalamic action on its own release or that of another possible PRL-releasing factor. When 3 micrograms VIP were injected into the third ventricle of conscious ovariectomized rats, a significant (P less than 0.005) and transient elevation of plasma oxytocin (OT) levels was observed. When OVX rats were injected iv with 1 ml anti-OT serum 30 min before the central administration of 3 micrograms VIP, the PRL surge seen after VIP injection in normal rabbit serum-treated controls was completely absent. The PRL surge seen after central VIP administration was not significantly altered by iv saline infusion (1 ml over 30 min) or by infusion of a VIP antagonist [D-4-Cl-Phe6,Leu17]VIP at a dose of 0.5 microgram/kg.min in 1 ml saline for 30 min before the VIP injection. This was not due to the inability of the VIP antagonist to block the PRL-releasing factor activity of VIP, since it significantly antagonized that action both in vitro and in vivo in the suckling stimulation paradigm. However, the PRL surge was completely absent in ovariectomized rats pretreated by iv infusion of an OT antagonist, [deamino Cys1,D-Trp2,Val4,Orn8]OT, at a similar dose. This recruitment of OT by VIP indicates that it may act at more than one locus within the hypothalamo-pituitary axis to insure the coordinated control of PRL secretion.
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PMID:Oxytocin mediates the hypothalamic action of vasoactive intestinal peptide to stimulate prolactin secretion. 291 3

We previously reported that the rat posterior pituitary contains a potent PRL-releasing factor (PRF) which is distinct from oxytocin (OT), TRH, and angiotensin II (AII). The objectives of this study were 1) to examine whether posterior pituitary extracts stimulate PRL release in the presence of dopamine (DA), 2) to determine the chemical nature of PRF, and 3) to estimate its mol wt. Perifused anterior pituitary cells were used to assess PRF activity. Posterior pituitaries and medial basal hypothalamus (MBH) fragments were extracted with perchloric acid and lyophilized. Subsequent to various treatments, samples were reconstituted in the perifusion medium and introduced to the cells in short pulses. Fractions were collected and analyzed for hormone content by RIA. During a constant infusion of DA (50 nM), PRL secretion was inhibited by 75%, yet the posterior pituitary extract retained its ability to rapidly stimulate PRL release. Studies using proteolytic enzymes showed that posterior pituitary PRF was resistant to inactivation by trypsin, whereas the PRF activity of AII was abolished. Both chymotrypsin and proline-specific endopeptidase significantly reduced the PRF activity in the posterior pituitary. The PRL-releasing activity of TRH was not affected by chymotrypsin. Immunoreactive vasoactive intestinal polypeptide was undetectable in posterior pituitary extracts. Oxidation of posterior pituitary extracts with performic acid caused only a modest reduction of their PRF activity, while the ability of OT to stimulate PRL release as well as immunoreactive OT was abolished. Studies using ultrafiltration membranes showed that the PRF activity in the posterior pituitary was less than 5,000 mol wt. Furthermore, posterior pituitary PRF partitioned in nearly equal amounts across 1K membranes, as did AII and OT. In contrast, about 80% of the PRF activity in the MBH and all of the synthetic TRH passed through the 1K membranes. We conclude that 1) posterior pituitary PRF can stimulate PRL secretion from perifused anterior pituitary cells in the presence of physiological concentrations of DA; 2) PRF is a small peptide(s) of less than 5,000, and perhaps closer to 1,000, mol wt; 3) PRF is resistant to inactivation by trypsin and to oxidation by performic acid, but is hydrolyzed by both chymotrypsin and proline-specific endopeptidase; and 4) these data further distinguish posterior pituitary PRF from known PRL secretagogues.
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PMID:Characterization of prolactin-releasing factor in the rat posterior pituitary. 313 Nov 18

The present study was designed to evaluate the possible physiological role of oxytocin (OXY) on PRL release by examining the effect of administration of potent pharmacological antagonists of OXY on the stimulation of PRL secretion observed in vitro from anterior pituitary (AP) cells in response to OXY administration or in a number of in vivo paradigms. OXY caused a dose-related increase in PRL release from dispersed AP cells and short term AP cell cultures which was blocked by administration of the OXY antagonists [1-deaminopenicillamine, 2-O-methyltyrosine, 8-ornithine]vasotocin (dPOMeOVT) or [1-(beta-mercapto-beta,beta-cyclopentamethylene propanoic acid)2-O-methyltyrosine, 8-ornithine]vasotocin (MPOMeOVT), respectively. The antagonists were given in vivo in a dose that completely blocked suckling-induced milk let-down for up to 90 min. Injection of the antagonists did not alter the 5-hydroxytryptophan-induced increase in plasma PRL or the increase associated with acute ether stress or acute suckling stimuli, suggesting that OXY is not a major component involved in the neuroendocrine mechanisms responsible for those particular increases. On the other hand, iv administration of dPOMeOVT or MPOMeOVT prevented the increase in plasma PRL normally observed on the afternoon of proestrus in the cycling female rat. The characteristic surge of LH was also blocked by high doses of these antagonists. These data demonstrate that PRL secretion undergoes a differential regulation, in that OXY appears to play a major role in regulating the increase in plasma PRL observed on the afternoon of proestrus, but apparently provides little, if any, contribution toward the neuroendocrine regulation of the increases in PRL associated with 5-hydroxytryptophan administration, acute ether stress stimulus, or acute suckling stimulus. The data also suggest that OXY receptors located in the AP that are involved in the OXY-induced increase in PRL release may be similar to those OXY receptors located in mammary and uterine tissue, since specific biological effects of OXY in those tissues are effectively blocked by the OXY antagonists dPOMeOVT and MPOMeOVT. A possible role of OXY neurons in the neural mechanisms triggering the LH surge during proestrus is also suggested.
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PMID:Role of oxytocin on prolactin secretion during proestrus and in different physiological or pharmacological paradigms. 333 12

The present study examines the effects of auditory stress on the plasma levels of pituitary hormones and cortisol. Each of twelve healthy male subjects participated in two experimental series; during one of them they were exposed to 85 dB(A) industrial noise from 9:00 to 21:00 h. Blood samples were taken by an indwelling venous catheter for 24 h at intervals of 20 min from 8:00 to 8:00 h. The plasma levels of ACTH, growth hormone, prolactin, oxytocin, vasopressin and cortisol were determined. In all subjects except one noise stress affected the profiles of the pituitary hormones but the responses were interindividually different. The oxytocin level was significantly elevated (p less than .01), ACTH also responded but less clearly, whereas the other hormones reacted only in individual cases. During the subsequent night sleep only PRL concentrations were elevated above the baseline plateau in several subjects. It was concluded that in humans the pituitary responses to noise stress are highly individual.
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PMID:Effects of daytime noise load on the sleep-wake cycle and endocrine patterns in man: II. 24 hours secretion of anterior and posterior pituitary hormones and of cortisol. 341 Jun 40

The presence of oxytocin (OT) in neuronal elements of the external layer of the median eminence and in hypophysial portal plasma suggests a role for the peptide in the control of anterior pituitary function. We have reported previously that OT stimulates PRL release in vitro; therefore, we attempted to establish evidence for a physiological PRL-releasing role for OT. Plasma OT levels rose significantly just before the PRL surges occurring during a suckling stimulus in lactating rats (10 min after pup reinstatement vs. 15 min for PRL) and 48 h after estrogen injection in ovariectomized (OVX) rats (at 1200 h vs. 1300 h). Dispersed anterior pituitary cells harvested from lactating female rats and OVX estrogen-primed rats released PRL in a specific, significant, and dose-related fashion when perifused in vitro with incubation medium containing 10(-7)-10(-9) M OT, doses similar to levels found previously in hypophysial portal plasma. Infusion of antiserum specific for OT into lactating females before pup reinstatement and into estrogen-primed OVX rats 2 h before the expected release of endogenous OT delayed and significantly reduced subsequent PRL surges compared to levels in saline-or normal rabbit serum-infused rats; however, PRL release was not completely abolished. These data indicate that OT plays a physiological role in the hypothalamic control of PRL secretion and further suggest the importance of multiple factors in coordinated regulation of PRL release.
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PMID:Evidence for a physiological role for oxytocin in the control of prolactin secretion. 373 36

Homogeneous preparations of decidual cells were obtained from term decidual tissue adherent to fetal membranes by using a slightly modified version of a technique developed for the isolation of decidual cells from first and second trimester decidua. The effects of human PRL (hPRL) and oxytocin on the kinetics of the hydrolysis of estrone sulfate were determined in decidual cells prepared from tissue obtained before and after the onset of labor. In addition, sulfatase activity in decidual cells isolated from term decidua was compared with those of chorionic cells isolated from chorion leave of the same pregnancy. Chorionic cells had significantly higher (mean, 2.5-fold) levels of sulfatase activity than the corresponding decidual cells. The mean sulfatase activity in decidual cells obtained after normal vaginal delivery [25 +/- 19 (+/- SE) nmol/mg protein X 15 min) was higher than that in decidual cells obtained from patients undergoing cesarean section before the onset of labor (1.7 +/- 0.11). This difference was significant (P less than 0.02, by Mann-Whitney test) in spite of the large variation in activity in preparations from vaginal deliveries. hPRL (500 ng/ml) and oxytocin (0.2 microM) had similar effects on sulfatase activity in decidual cells in a manner dependent on whether the cells were isolated from tissue obtained before or after labor. In cells isolated from fetal membranes obtained before labor (cesarean delivery), hPRL or oxytocin significantly stimulated sulfatase activity, whereas in decidual cells obtained after vaginal delivery, both hPRL and oxytocin significantly inhibited sulfatase activity. The Michaelis constants for the hydrolysis of estrone sulfate (Km, 22 +/- 4.8 microM) were not affected by these hormones. Since the mean sulfatase activity of decidual cells obtained before labor was approximately 10-fold higher than the activity reported for endometrial stromal cells, PRL produced by decidual cells may act in vivo as an autocrine factor to stimulate their sulfatase activity.
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PMID:In vitro effects of human prolactin and oxytocin on sulfatase activity in isolated human decidual cells. 373 40

Levels of oxytocin (OT) and PRL were measured in plasma drawn before and during intermittent mechanical pump and tactile stimulation of the breast in five normal cycling women and 19 women in the third trimester of pregnancy. OT was significantly increased above baseline in response to breast stimulation in two of five cycling women and PRL increased in one of the two OT responders. In pregnant women, mean OT post nipple stimulation was significantly higher than pre nipple stimulation whereas PRL did not increase significantly. The response of OT to nipple stimulation occurred in 18 of 19 pregnant women compared to only two of five normal cycling women but the magnitude of the OT response in pregnant women was less than in cycling women or post-partum lactating women previously studied in this laboratory. In one non post-partum woman who induced lactation for the purpose of breast-feeding an adopted infant, OT and PRL were measured before and during mechanical pump and tactile stimulation before initiation of breast-feeding. OT increased during mechanical pump and tactile stimulation of the breast, as well as suckling, whereas PRL increased only in response to suckling. Levels of LH were measured in plasma every 20 min for 160 min at the following times: before initiation of breast-feeding, during induced lactation while breast-feeding, and 30 d after discontinuation of breast-feeding. Despite the development of oligomenorrhoea during the period of breast-feeding, levels of progesterone were not suppressed and LH was released in a normal pulsatile fashion.
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PMID:Breast stimulation in cycling women, pregnant women and a woman with induced lactation: pattern of release of oxytocin, prolactin and luteinizing hormone. 379 64

We studied prospectively eight healthy postpartum breast-feeding women for 6 months during early, middle, and late lactation. Blood for measurement of oxytocin (OT), PRL, and arginine vasopressin was drawn before and every 3 min from each women during 15 min of infant suckling for two consecutive feedings during each stage of lactation. Basal plasma OT was not different in breast-feeding [0.7 +/- 0.1 (+/- SEM) microU/ml] and nonbreast-feeding women (0.8 +/- 0.2 microU/ml). OT increased significantly in response to infant suckling (P less than 0.00001) to 5.9 +/- 0.5 microU/ml and remained elevated throughout a feeding. OT was released during infant suckling in an episodic pattern in some, but not all, women; peak OT varied among women (5.0-23.3 microU/ml). There was no significant difference in the mean stimulated OT or the pattern of release comparing the first and second feedings of the same day. The mean OT (n = 8) released during 15 min of infant suckling was not significantly different in early (3.9 +/- 0.3 microU/ml), middle (4.5 +/- 0.3 microU/ml), and late (5.8 +/- 0.4 microU/ml) lactation. In the four women who breast fed exclusively, the mean stimulated OT was significantly higher (P less than 0.01) during late lactation (8.6 +/- 0.4 microU/ml) vs. early (4.6 +/- 0.4 microU/ml) or middle (6.1 +/- 0.4 microU/ml) lactation. In the other four women who provided formula supplements, OT did not change. Plasma arginine vasopressin did not increase in response to infant suckling. Plasma PRL increased in response to infant suckling, reaching a peak at 15 min. Mean basal PRL decreased progressively from weeks 1-24 postpartum. Mean peak PRL decreased significantly from early (162 +/- 29) to middle (130 +/- 15) to late (77 +/- 10) ng/ml lactation (P less than 0.05). OT release in response to infant suckling continues throughout the first 6 months postpartum in breast-feeding women, and the pattern is reproducible. The maximum release of OT is dependent upon continuous regular nipple stimulation. In contrast to basal and suckling-induced levels of PRL, which decreased with time postpartum, basal and suckling-induced OT release did not decrease from early to late lactation.
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PMID:A prospective longitudinal study of the release of oxytocin and prolactin in response to infant suckling in long term lactation. 394 49

The widespread occurrence of opioid peptides and their receptors in brain and periphery correlates with a variety of actions elicited by opioid agonists and antagonists on hormone secretion. Opioid actions on pituitary and pancreatic peptides are summarized in Table 1. In rats opioids stimulate ACTH and corticosterone secretion while an inhibition of ACTH and cortisol levels was observed in man. In both species, naloxone, an opiate antagonist, stimulates the release of ACTH suggesting a tonic suppression by endogenous opioids. In rats, a different stimulatory pathway must be assumed through which opiates can stimulate secretion of ACTH. Both types of action are probably mediated within the hypothalamus. LH is decreased by opioid agonists in many adult species while opiate antagonists elicit stimulatory effects, both apparently by modulating LHRH release. A tonic, and in females, a cyclic opioid control appears to participate in the regulation of gonadotropin secretion. Exogenous opiates potently stimulate PRL and GH secretion in many species. Opiate antagonists did not affect PRL or GH levels indicating absence of opioid control under basal conditions, while a decrease of both hormones by antagonists was seen after stimulation in particular situations. In rats, opiate antagonists decreased basal and stress-induced secretion of PRL. Data regarding TSH are quite contradictory. Both inhibitory and stimulatory effects have been described. Oxytocin and vasopressin release were inhibited by opioids at the posterior pituitary level. There is good evidence for an opioid inhibition of suckling-induced oxytocin release. Opioids also seem to play a role in the regulation of vasopressin under some conditions of water balance. The pancreatic hormones insulin and glucagon are elevated by opioids apparently by an action at the islet cells. Somatostatin, on the contrary, was inhibited. An effect of naloxone on pancreatic hormone release was observed after meals which contain opiate active substance. Whether opioids play a physiologic role in glucose homeostasis remains to be elucidated.
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PMID:Endocrine actions of opioids. 608 80


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