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

We previously reported that prolactin (PRL) could increase the activity of ornithine decarboxylase (ODC) in liver slices taken from larval tiger salamanders (Ambystoma tigrinum). This action of the hormone was inhibited by oxytocin (OT), the calcium ionophore A23187, and diacyglycerol (DG) and was duplicated by 10 microM verapamil (VML), a calcium channel blocker. Here, we expand these results to show that 1) a higher dose of VML (50 microM) produces an additive effect with PRL; 2) addition of small amounts of calcium (0.1 mM) to the liver culture medium blocks PRL action; 3) neither nifedipine (NIF), a different type of calcium channel blocker, nor EDTA alter PRL action; and 4) gossypol, a reported inhibitor of protein kinase C, mimics PRL action. Additionally, we show that PRL increases ODC activity in tiger salamander tail skin in vitro, a tissue previously demonstrated to be a PRL target tissue in this species. The same set of treatments which we have shown to modify PRL effects on ODC in liver slices affects PRL action in the tail skin in a parallel manner. Thus, the mechanism whereby PRL enhances ODC activity appears to be the same in both these tissues. These results are discussed in conjunction with the findings from similar studies using mammalian tissues in an attempt to assess the current picture of the mechanism of PRL action and the possible role of inositol phospholipid turnover, calcium, and protein kinase C in the action of this hormone.
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PMID:Reduced calcium and inhibition of protein kinase C mimic the enhancement of ornithine decarboxylase activity of prolactin in Ambystoma tigrinum tissues. 194 Aug 22

The effect of several growth factors, protein and steroid hormones on follicle stimulating hormone (FSH)-stimulated and basal inhibin secretion by mature porcine granulosa cells (g-cells) in culture was examined in order to elucidate the putative role of growth factors and hormones in the regulation of inhibin secretion by porcine g-cells in vitro. Cells were incubated with the respective hormones over a timespan of 0-144 h and immunoreactive inhibin was measured with a radioimmunoassay against porcine inhibin. Epidermal growth factor (EGF) and human transforming growth factor type beta (TGF-beta) decreased basal and gonadotrophin-stimulated inhibin and progesterone in a dose-dependent manner. In the absence of insulin, insulin-like growth factor type I (IGF-I) caused a 4-fold enhancement of basal inhibin secretion, but inhibin secretion was elevated only to 20% above control in the presence of 500 nM insulin. Porcine platelet-derived growth factor (PDGF) had no significant effect on basal or FSH-induced inhibin secretion by g-cells. In addition, neither gonadotrophin-releasing hormone (GnRH) nor prolactin (PRL), arginine vasopressin (AVP) and oxytocin affected basal or FSH-stimulated inhibin release by porcine g-cells. Oestradiol caused a slight but significant (P less than 0.01) rise of basal inhibin production (158% of control) in the last 2 days of culture (96-144 h) and the effect of androstenedione on basal (158% of control) and FSH-stimulated (140% of control) inhibin release (P less than 0.01) was also only visible on Days 4-6 of culture. In contrast to androstenedione and oestradiol, progesterone did not show any effect during 6 days of culture in a dose range of 10(-5) to 10(-9) M. Like steroids, prostaglandin E2 (PGE2) had a stimulatory effect on basal inhibin production (250% of control) by porcine g-cells, visible on Days 3-6 of culture, but an inhibitory effect on FSH-stimulated release (less than 40% of control). Over all the experiments with different hormones and growth factors, tested in varying doses and over a time span of 0-144 h, there was a strong correlation between progesterone and inhibin secretion by g-cells (0-48 h = 0.78; 48-96 h = 0.92; 96-144 h = 0.92). These results suggest that EGF, TGF-beta, IGF-I, oestradiol and androstendione as well as PGE2 have para- and/or autocrine modulatory effects on basal and FSH-stimulated inhibin secretion by mature porcine g-cells in vitro and further demonstrate that the secretion of the proteohormone inhibin and the steroid progesterone are closely related.
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PMID:Effects of growth factors and hormones on basal and FSH-stimulated inhibin production by porcine granulosa cells in vitro. 194 20

The neurotransmitter histamine (HA) participates in the neuroendocrine regulation of pituitary hormone secretion and in the regulation of some peripheral hormones. In general, HA has a stimulatory but indirect effect on the release of these hormones by activation of postsynaptic receptors in the hypothalamic region. The release of the pro-opiomelanocortin-derived peptides ACTH, beta-endorphin (beta-END), and alpha-melanocyte-stimulating hormone (alpha-MSH) occurs by stimulation of H1- and H2-receptors and seems to be mediated via release of corticotropin-releasing hormone and vasopressin from the hypothalamus. The HA-induced release of prolactin (PRL) involves H2-receptors in some hypothalamic areas and H1-receptors in other areas. The release of PRL occurs by histaminergic inhibition of tuberoinfundibular dopaminergic neurons and by stimulation of serotoninergic and vasopressinergic neurons. Histaminergic neurons seem to participate in the mediation of the stress-induced release of ACTH, beta-END, alpha-MSH, and PRL. The neurohypophysial hormones vasopressin and oxytocin are stimulated by HA, and a physiological role of HA in the control of vasopressin secretion is likely. HA stimulates the release of peripheral catecholamines and renin. The stress-induced increase in plasma catecholamines and plasma renin activity (PRA) seems also to involve central histaminergic neurons. The effect of HA and stress on peripheral catecholamines is mediated via H1- and H2-receptors, while that on PRA is mediated via H2-receptors.
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PMID:Neuroendocrine functions of histamine. 205 12

Maintenance of corpus luteum (CL) function is essential for establishment of pregnancy in mammals. Estrogens from pig conceptuses (embryo and associated membranes) initiate events that, with prolactin, redirect secretion of the uterine luteolytic hormone prostaglandin F2 alpha (PGF) from an endocrine (to uterine veins) to an exocrine (to uterine lumen) direction to prevent luteolysis. Ovine conceptuses secrete ovine trophoblast protein-1 (oTP-1), which exhibits high amino acid sequence relatedness with alpha II interferons (IFN alpha II) and inhibits synthesis of endometrial receptors for oxytocin and uterine production of luteolytic pulses of PGF. Estrogens and oTP-1 are local antiluteolytic signals to endometrium, whereas human chorionic gonadotrophin (hCG) appears to have a direct luteotrophic effect on CL. A progestational endometrium secretes proteins that serve as growth factors, transport proteins, regulatory proteins and enzymes, as well as transporting nutrients into the uterine lumen to support conceptus development.
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PMID:Comparative aspects of conceptus signals for maternal recognition of pregnancy. 206 81

In order to elucidate the possible involvement of endothelin-1 (ET-1) in the development of the feto-placental unit, plasma concentrations of immunoreactive ET-1 during pregnancy and delivery were measured in the current study. Forty-four pregnant women (8 in the 1st trimester, 8 in the 2nd trimester, 12 in the 3rd trimester and 16 at delivery), 6 at 1 month postpartum and 14 non-pregnant women volunteered to participate in this study. Plasma levels of immunoreactive ET-1 in all subjects were measured by specific radioimmunoassay. Plasma cortisol, prolactin and oxytocin levels during delivery were also measured by RIA. Although plasma ET-1 levels did not change during the 1st (1.3 +/- 0.4 pg/ml, mean +/- S.E.M., n = 8) or 2nd (1.7 +/- 0.3 pg/ml, n = 8) trimester, they were significantly (p less than 0.05) higher in the 3rd trimester (2.6 +/- 0.3 pg/ml, n = 12) than those of the non-pregnant controls (1.7 +/- 0.3 pg/ml, n = 14) and returned to the control levels within 1 month post-partum (1.8 +/- 0.1 pg/ml, n = 6). Maternal ET-1 levels before labor onset (2.3 +/- 0.4 pg/ml, n = 16), at delivery (3.0 +/- 0.7 pg/ml) and 24 hours post-partum (2.7 +/- 0.5 pg/ml) showed no significant differences among them. On the other hand, ET-1 levels in cord plasma (7.0 +/- 1.2 pg/ml) were significantly higher (p less than 0.05) than those in maternal plasma. Furthermore, there were no significant correlations between plasma ET-1 levels and those of other hormones (cortisol, prolactin and oxytocin) during delivery. From these results, we concluded that maternal plasma ET-1 levels significantly increased in the last trimester and returned to non-pregnant levels within one month post-partum.
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PMID:[Levels of endothelin-1 in maternal and cord plasma during pregnancy and delivery]. 206 12

Experimental sows were divided into three groups treated as follows: Group I (n = 3): on Day 12 of the oestrous cycle i.m. injection of oxytocin (OT) at a dose of 0.25 I.U./kg b.w.; Group II (n = 4): on Day 12 and 13 of the oestrous cycle i.v. injections of OT (0.03 I.U./kg b.w.), and Group III (n = 3): on Day 13 of the oestrous cycle i.m. injection of cloprostenol (prostaglandin F2 alpha analogue; PG) at a dose of 500 micrograms. Blood samples were collected from the jugular vein for 2 h before and 2 h or 4 h after OT and PG treatment, respectively. Concentration of prolactin (PRL) was determined in all studied groups, whereas 13,14-dihydro-15-keto-PGF2 alpha (PGFM) was estimated in Group I and II. OT injections (i.v. or i.m.) Day 12 and 13 of the oestrous cycle raised its concentrations in the peripheral blood lasting for 50 and 120 min, respectively. But short lasting rise of PRL was caused by OT in 3 sows, whereas of PGFM in 2 sows only. In all other studied sows values of PRL and PGFM were during an experiment on the pre-treatment level. However, if PGF2 alpha analogue was injected on Day 13 of the cycle, it caused significant rise of PRL concentration (P less than 0.01) 20 min after treatment. PRL concentration measured after PG administration (7.0 +/- 0.7 ng/ml) was statistically higher (P less than 0.01) compared to the period proceeding PG injection (2.6 +/- 0.3 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of oxytocin and PGF2 alpha on prolactin release in sows. 208 65

The roles of oxytocin (OT) and vasopressin (AVP) on both basal and estrogen-induced prolactin (PRL) secretion were examined. Adult female Sprague-Dawley rats that were ovariectomized for 3 weeks and received estrogen treatment for 1 week were used. Intravenous administration of hormones and serial blood sampling were accomplished through indwelling intraatrial catheters which were implanted two days before. Plasma PRL levels were measured by radioimmunoassay. Oxytocin at a dose of 20 micrograms/rat stimulated a moderate PRL release in the morning and lower doses (5 and 10 micrograms) were without effect. Vasopressin was most effective at a dose of 5 micrograms/rat in stimulating PRL release, while consecutive injections of higher doses (10 and 20 micrograms) were less effective. In contrast, TRH, ranging from 1 to 8 micrograms/rat, induced a dose-dependent increases in PRL secretion. Using the effective dosages determined from the morning studies, repeated injections of either OT, AVP or their specific antagonists MPOMeOVT [( 1-(beta-mercapto-beta, beta-cyclopentamethylene propanoic acid), 2-(O-methyl)tyrosine, 8-ornithine]-vasotocin) and d (CH2)5Tyr(Me)AVP ([1-(beta-mercapto-beta, beta-cyclo-pentamethylene propionic acid), 2-(O-methyl)tyrosine, 8-arginine]-vasopressin), were given hourly between 1300 to 1800 h and blood samples were obtained hourly from 1100 to 1900 h. It was found that either OT or AVP significantly reduced the afternoon PRL surge, while their antagonists were not as effective. When OT or AVP were administered together with their specific antagonists, the inhibitory effects of either hormone on PRL surge were reversed. Thus it is concluded that both OT and AVP assume a non-specific stress-like effect on PRL release, in which basal secretion is stimulated and surge secretion is inhibited.
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PMID:Paradoxical effects of oxytocin and vasopressin on basal prolactin secretion and the estrogen-induced prolactin surge. 212 15

The responses of the adenohypophyseal hormones adrenocorticotrophin (ACTH), growth hormone (GH), thyroid stimulating hormone (TSH), prolactin, luteinizing hormone (LH) and follicle stimulating hormone (FSH) to sub-maximal doses of hypothalamic releasing factors were studied in six lean male volunteers (age 23-35 years) with and without infusions of oxytocin (OXT). OXT infusion (mean plasma concentration 133.6 +/- 2.6 pmol/l) completely inhibited the plasma ACTH responses to corticotrophin releasing hormone (CRH) (saline, peak increment ACTH 1.61 +/- 0.75 pmol/l; OXT, peak increment ACTH - 0.04 +/- 0.28 pmol/l; P less than 0.05). OXT infusion had no significant effect on the GH response to growth hormone releasing hormone (GHRH), the TSH and prolactin responses to thyrotrophin releasing hormone (thyroliberin, TRH) or the LH and FSH responses to gonadotrophin releasing hormone (luteoliberin, GnRH). The data support a role for OXT in the modulation of ACTH secretion in man.
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PMID:The effect of oxytocin infusion on adenohypophyseal function in man. 216 Aug 73

The effects of an opioid receptor antagonist, naloxone (NAL), were studied on the changes in pituitary hormone secretion induced by emotional stress. Male Wistar rats were trained with tone stimuli paired with electric footshocks and tested with the tone and environmental cue signals for emotional stress of fear acquired by learning as described previously (Onaka et al. 1988). Rats received s.c. injected NAL 30 min before testing at doses of 0, 0.2, 1.0, 5.0 and 25.0 mg/kg b.w. Half the rats were injected with 0.5 M NaCl (20 ml/kg b.w.) together with NAL. In these hypertonic rats plasma vasopressin level was slightly increased after NAL. The increment was statistically significant in control groups but not in experimental groups. However the suppression of vasopressin secretion by emotional stimuli was not changed by NAL. Plasma oxytocin levels were extremely high and not significantly different among experimental, unshocked control and untested control groups. NAL further increased the oxytocin level dose-dependently. NAL did not significantly change plasma adrenocorticotrophic hormone (ACTH) levels and hence did not modify the augmentative response in ACTH secretion to emotional stimuli. Plasma prolactin level was significantly elevated after emotional stimuli and NAL depressed the prolactin level in each of experimental and control groups. After NAL, the magnitude of the facilitatory response in prolactin secretion to emotional stimuli was decreased. Motor activity and its suppressive response to emotional stimuli were not influenced by NAL. In another half of rats under a normal osmotic condition the vasopressin response to emotional stimuli was not affected by NAL. NAL further augmented potentiation of oxytocin secretion after emotional stimuli dose-dependently.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of naloxone on neuroendocrine responses to fear-related emotional stress. 216 20

Postpartum infertility is caused by four factors: general infertility, lack of uterine involution, short estrous cycles and anestrus. The general infertility component is common to any estrous cycle and reduces potential fertility by 20 to 30%. Incomplete uterine involution prevents fertilization during the first 20 d after calving but is not related to anestrus. Short estrous cycles prevent fertility during the first 40 d after calving by causing the cow to return to estrus before pregnancy recognition occurs. Anestrus is the major component of postpartum infertility and is affected by several minor factors: season, breed, parity, dystocia, presence of a bull, uterine palpation and carryover effects from the previous pregnancy as well as two major factors: suckling and nutrition. These major factors have direct effects on anestrus but also interact with one or more other factors to control postpartum anestrus. Physiological mechanisms associated with anestrus involve blockage of the GnRH "pulse generator" in the hypothalamus, but other pathways also must be involved because bypassing the pulse generator is not an effective treatment for all cows. The primary cause of anestrus probably is different for different stages of anestrus. The mediating mechanisms for anestrus are not involved with prolactin, oxytocin, the adrenal or direct neural input from the mammary gland but are at least partially involved with blood glucose and the endogenous opioid peptide system. Management options to decrease the impact of anestrus and infertility include: 1) restrict breeding season to less than or equal to 45 d; 2) manage nutrition so body condition score is 5 to 7 before calving; 3) minimize effects of dystocia and stimulate estrous activity with a sterile bull and estrous synchronization; and 4) judicious use of complete, partial or short-term weaning.
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PMID:Physiological mechanisms controlling anestrus and infertility in postpartum beef cattle. 218 Aug 77


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