UNIPROT:P01178 - FACTA Search

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

The bovine CL is one of the sites for the production of prostaglandins (PG). Although many in vitro models, mainly using dispersed luteal cell incubations, have shown the variety of CL responses to PGs (luteotropic, no effect, or luteolytic), the functional role of luteal PGs in cattle remains to be elucidated. Therefore, the aim of the present study was to examine the effects of PGs with respect to progesterone (P4) and oxytocin (OT) release from the bovine CL in vitro (Days 8-12 of the estrous cycle) via a microdialysis system (MDS), in which intact cell-to-cell contact exists. Thirty-minute perfusion with PGF2 alpha, PGE2, and PGI2 (10(-10)-10(-5) M) induced significant, but different, acute effects. PGF2 alpha and PGE2 clearly stimulated hormone (P4 and OT) release, while PGI2 slightly inhibited hormone secretion during infusion at low doses but stimulated secretion at 10(-6) and 10(-5) M concentrations. Additionally, catabolized PGF2 alpha and PGI2 (13,14-dihydro-15-keto-PGF2 alpha [PGFM] and 6-keto-PGF1 alpha, respectively) induced responses different from those of the original PGs; both PGFM and 6-keto-PGF1 alpha at low doses weakly inhibited P4 release, but at 10(-5) M concentration stimulated release. Phorbol 12-myristate 13-acetate (TPA), a potent stimulator of the protein kinase C (PKC) system in bovine luteal cells, stimulated P4 and OT release when administered alone. Pre-exposure with TPA (10(-9) M) for 2.5 h resulted in an increase in the stimulative potency of PGF2 alpha and PGI2, but not of PGE2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute actions of prostaglandin F2 alpha, E2, and I2 in microdialyzed bovine corpus luteum in vitro. 837 69

The aim of the present study was to investigate the presence of the immunoreactive oxytocin in human placental extracts and putative factors regulating the release of immunoreactive oxytocin from cultured human placental cells. Fresh placental tissue was collected from pregnant women at term and dissected of membranes (n = 5). Presence of immunoreactive oxytocin in trophoblast tissue was evaluated by a specific radio-immunoassay after acidic extraction and high-pressure liquid chromatography. In a second set of experiments, primary cultures of placental cells were performed and, 48-72 h after dissociation, the effect of arginine vasopressin, corticotropin-releasing factor, neuropeptide Y, activin A, inhibin A, noradrenaline or prostaglandins on immunoreactive oxytocin level in culture medium was investigated. The presence of immunoreactive oxytocin was shown in the acidic extract of trophoblast at term, and in the culture medium of human placental cells, and it was identical to the native peptide. The addition of corticotropin-releasing factor or arginine vasopressin, but not of neuropeptide Y, increased the release of immunoreactive oxytocin three- to fourfold from placental cells, with a dose-dependent effect (P < 0.01). A significantly increased release of immunoreactive oxytocin was shown in presence of noradrenaline (P < 0.01), which was reversed by prazosin, an antagonist of alpha-adrenergic receptors. Recombinant human activin A (P < 0.01), but not inhibin A, stimulated the release of immunoreactive oxytocin three- to fourfold from placental cells. Prostaglandin F2 alpha was a potent secretagogue of immunoreactive oxytocin, whereas a partial or no effect was observed when prostaglandin E2 or prostaglandin I2 was added. Thus, the present findings showed that human placenta contains immunoreactive oxytocin, and that its release from cultured placental cells is regulated by neurohormones, growth factors or prostaglandins.
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PMID:Activin A, corticotropin-releasing factor and prostaglandin F2 alpha increase immunoreactive oxytocin release from cultured human placental cells. 882 13

The aim of the investigation was to evaluate the possible action of prostaglandins (PGs) and oestradiol-17 beta (oestradiol) on the specific binding for oxytocin in bovine luteal cells. Cultured cells of bovine corpora lutea at the mid-luteal stage (Day 8-12 of the oestrous cycle) were examined for the presence of oxytocin receptors by a radioreceptor assay using the 125I-labelled oxytocin antagonist [d(CH2)5,Tyr(Me)2,Thr4,Tyr-NH29]-vasotocin (125I-OVT) as a ligand. The cells were cultured for 48 h in total. In the final 15 h of culture, the luteal cells were exposed to varying concentrations of PGF2 alpha, PGE2 and/or oestradiol. After culture, the cells were incubated with 37,000 dpm (0.5 nM) 125I-OVT with or without 100 nM of unlabelled oxytocin. PGF2 alpha, at 10(-8) M and 10(-7) M, stimulated the specific binding for oxytocin to levels as high as 128% of controls (P < 0.01); by contrast, PGE2, PGI2 or oestradiol had no effect on oxytocin binding. Scatchard analysis revealed that the concentration of oxytocin receptors was increased (P < 0.05) from 6.7 fmol micrograms-1 DNA to 8.4 fmol micrograms-1 DNA by stimulation with 10(-7) M of PGF2 alpha without changing the binding affinity. No further increase in the specific binding was observed when PGF2 alpha was used in combination with PGE2, PGI2 or oestradiol at a concentration of 10(-7) M. Addition of indomethacin (28 microM) resulted in the inhibition of PGF2 alpha secretion, coinciding with a significant decrease in oxytocin binding (P < 0.01). However, addition of arachidonic acid (100 microM) caused a significant increase in the secretion of PGF2 alpha and the specific binding for oxytocin concomitantly (P < 0.05). When the protein kinase C (PKC) activity of the luteal cells was inactivated by preincubating cells for 13 h with 1 microM phorbol 12-myristate 13-acetate before PGF2 alpha stimulation, the specific binding for oxytocin was not affected by PGF2 alpha stimulation (10(-7) M) in the final 15 h of culture. These data suggest that PGF2 alpha may be one of the potent regulators for luteal oxytocin receptors in a paracrine and/or autocrine manner, and that its action is mediated by PKC.
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PMID:Effects of prostaglandins and oestradiol-17 beta on oxytocin binding in cultured bovine luteal cells. 884 69

Although milk yield of cows and goats is known to be closely related to the total flow of blood through the udder, a number of studies suggest that milk yield can vary independently. No studies have attempted to measure the proportion of total flow that is nutritive. Within the mammary gland, capillary networks form a basket-like architecture surrounding each alveolus. Notably, flow in individual capillaries is not constant and varies among capillaries. Capillary flow (measured by intravital microscopy) was decreased by oxytocin, which generally increased total flow in the mammary artery, suggesting that the proportion of total flow that is nutritive can vary. In addition to classic metabolic regulators (e.g., carbon dioxide and oxygen) of tissue blood flow, the mammary gland produces a number of vasodilatory compounds, including parathyroid hormone-related protein, insulin-like growth factor-I, prostacyclin, nitric oxide, and endothelin. All of these compounds have been shown to alter mammary blood flow. Mammary tissue also contains kallikrein and angiotensin-converting enzyme, which convert circulating kinins and angiotensin, respectively, into potent vasoactive compounds. A number of these compounds are produced by epithelial cells themselves, providing a mechanism for the functioning epithelium to control its own blood supply and, hence, nutrient flow for milk synthesis. In this review, we examine the nature of the mammary microcirculation, its behavior under different conditions, and some of the regulatory features of the mammary microvasculature.
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PMID:Regulation of blood flow in the mammary microvasculature. 887 13

Secretion of progesterone in vitro by mature day 8 ovine corpora lutea (CL) of the estrous cycle was increased linearly by ovine LH (1, 10 and 100 ng/ml) or prostaglandin E2 (PGE2) 1, 10 and 100 ng/ml) in a dose dependent manner (P < or = 0.05). Progesterone secretion in vitro by 88-90 day ovine CL of pregnancy was not affected P > or = 0.05 by LH (1, 10 and 100 ng/ml) while prostaglandin E1 (PGE1) 1, 10 and 100 ng/ml) increased (P < or = 0.05) secretion of progesterone in a dose dependent manner and PGE2 (1, 10 and 100 ng/ml) increased (P < or = 0.05) secretion of progesterone only at the 100 ng/ml dose. Day 8 ovine CL of the estrous cycle did not secrete (P > or = 0.05) detectable quantities of prostaglandin F2 alpha (PGF2 alpha) or prostaglandin E (PGE) while 88-90 day ovine CL of pregnancy secrete PGE (P < or = 0.05) but not PGF2 alpha (P > or = 0.05). Regulation of PGE secretion by 88-90 day ovine CL of pregnancy may be via pregnancy specific protein B (PSPB), which increased (P < or = 0.05) PGE and progesterone but not PGF2 alpha (P > or = 0.05) secretion. Secretion of progesterone by CL of 88-90 days of pregnancy was not affected by IGF1, IGF2, PAF-16, PAF-18, oxytocin, PGI2, PGD2 or leukotriene C4 (P > or = 0.05). It is concluded that PGE1 or PGE2 but not LH regulates secretion of progesterone in vitro by 88-90 day ovine CL of pregnancy. In addition, it is concluded that 88-90 day ovine CL of pregnancy secretes it's own luteotropin, which is PGE. Secretion of PGE by ovine CL of pregnancy may be regulated by PSPB.
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PMID:PGE1 or PGE2 not LH regulates secretion of progesterone in vitro by the 88-90 day ovine corpus luteum of pregnancy. 924 73

We describe the case of a pregnant woman, 35 weeks' gestation, with primary pulmonary hypertension and coarctation of the aorta requiring emergency Caesarean section under general anaesthesia. The patient had a pulmonary artery catheter inserted before operation which revealed pulmonary artery pressures in excess of 80/40 mm Hg. These were lowered using an infusion of glyceryl trinitrate. After delivery of the baby and administration of oxytocin, pulmonary artery pressures were more difficult to control. An infusion of prostacyclin was substituted which stabilized pulmonary pressures. After operation, she was transferred to the intensive care unit where prostacyclin was administered by an "aerosolized" route. Her trachea was extubated after 48 h and she made an uneventful recovery.
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PMID:Anaesthesia for caesarean section in the presence of severe primary pulmonary hypertension. 1053 69

The regulation of aquaporin-2 (AQP2) water channel excretion in the collecting duct depends mainly on the action of vasopressin (AVP). Recently, however, other regulatory factors have been identified: atrial natriuretic factor, oxytocin and prostaglandins. In healthy volunteers (5 males, 5 females; mean age 23 +/- 3 years) we therefore evaluated the effect of a stable analogue of prostacyclin-2 (PGI(2)), iloprost, on renal function and on the urinary excretion of AQP2 (U-AQP2). After 6 h of iloprost infusion, U-AQP2 increased from 0.8 +/- 0.15 to 1.8 +/- 0.2 pmol/mg creatinine (p < 0.001), while the urinary flow rate increased from 1.4 +/- 0.2 to 1.8 +/- 4 (p < 0.01). No significant change was found in the AVP serum concentration, with a basal value of 3.17 +/- 0.12 vs. 3.15 +/- 0.12 pg/ml after 6 h of prostacyclin infusion. All the values returned to pre-study levels after a recovery period of 6 h. In conclusion, the PGI(2) analogue, iloprost, can induce U-AQP2 excretion independent of AVP.
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PMID:Effect of a prostacyclin analogue, iloprost, on urinary aquaporin-2 excretion in humans. 1205 53

The low postpartum levels of PGI2 interacting with oxytocin vis-a-vis myometrial contractility may prevent postpartum hemorrhage. Predisposing factors for atonic postpartum bleeding are uterine overdistension, grand multiparity, prolonged labor, anemia, toxemia, and heavy narcosis. Routine administration of oxytocic agents reduce uterine atony. In 1 group of 40 patients .2 mg methyl ergometrine given iv postplacentally produced less bleeding than in the other group of 40 getting placebo. 1 mg of iv PGE1, .2 mg ergometrine, 3 IU oxytocin or a combination of PGE1 and ergometrine was compared in 180 women. PGE1 did not reduce blood loss. PGF2alpha was used successfully to induce labor in 21 women reducing blood loss compared to oxytocin. Another 10 women received in syntometrine and 5 got im .25 mg sulprostone at the moment of crowning, and the latter reduced postpartum blood loss. 90 women in 3 groups of 30 each at high risk of hemorrhage were injected im .2 mg methyl ergometrine maleate, .25 mg 15-methyl-PGF2alpha, and .5 mg sulprostone, respectively, resulting in prevention of severe hemorrhage. Intramyometrial injection of .5-1 mg of PGF2alpha induced uterine contractions and controlled bleeding in atonic hemorrhage when oxytocin failed. 20 mg PGE2 vaginal suppositories controlled postpartum atony after cesarean section, although fever and hypotension did occur. Im 15-methyl-PGF2alpha proved superior in producing hemostasis to intramyometrial PGF2alpha injection. In 2 studies .25 mg of 15-methyl-PGF2alpha was injected at 1.5 hour intervals arresting hemorrhage in 15 out of 16 and 18 out of 20 cases, respectively. Intrauterine infection caused all 3 failures. Sulprostone by infusion of 1.7-30 mcg/min or by 500 mcg im injection also controls postpartum hemorrhage.
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PMID:The use of prostaglandins in post-partum haemorrhage. 1231 32

Regulation of myometrial functions during gestation, labor and birth are in the forefront of research in reproductive sciences. The complexity of the problem is reflected by our scant understanding of the intimate cellular and molecular events underlying these phenomena, despite extensive efforts spanning several decades. Unlike other smooth muscles, the myometrium is, to a large extent, under hormonal control. Of these, the steroid hormones, progesterone and estrogen, play dominant roles in terms of uterine growth, the maintenance of quiescence during gestation and the preparation of the uterus for labor and delivery. In addition to steroid hormones, there are a number of factors that modulate myometrial contractility (oxytocin, prostaglandins, endothelin, platelet activating factor) and relaxation (corticotropin releasing hormone, prostacyclin, nitric oxide). Although notable advances have been made towards understanding some of the key steps in receptor signaling that define the actions of these factors, a good deal of new information is needed to fully understand this fundamental life process. Pharmaceutical agents have been used extensively to induce labor or to prolong pregnancy in the case of preterm labor that represents the major cause of perinatal morbidity and mortality. Because preterm labor is a syndrome of multiple etiologies, pharmacologic agents will have to be targeted accordingly. This review attempts to present a critical overview of these topics.
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PMID:Regulation of myometrial smooth muscle functions. 1532 Jul 59

Factors which induce the corpus luteum persistent (CLP) creation in animal ovaries are located in the hypothalamic-pituitary-ovarian axis and also in the uterus. In cows and likewise in others animals, various mediators of inflammatory reaction are released, mainly proinflammatory cytokines from inflamed uterus into the blood and lymph. Afterwards the cytokines cross the blood-brain barrier, and though the brain mediators alter the hormonal profile and amplitude pulses of the hormones release in the hypothalamus and the pituitary. Until it is known, that cytokines: IL-1, IL-2, IL-6, TNF-alpha and also IFN-alpha, administered into the median eminence, cause an increase in corticotrophin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) concentrations and decrease in the pituitary gland hormones secretion. The immune system, represented in the corpora lutea (CL) by numerous macrophages/monocytes, limphocytes and neutrophils plays an important role in the luteolysis process. The stimulating factor of the infiltration of these cells is an increased PRL level. The preovulatory increase in PRL level regulates the number of macrophages in newly-formed CL and later influences the number of these cells in the luteolysis period. The pulsatory release and high levels of the hypophyseal oxytocin (OT) and uterine PGF2alpha ensure the beginning and the normal course of the luteolysis period. The cytokines decrease OT concentration and disorder its pulsatory release from the pituitary. In these circumstances the quantity of the uterine PGF2alpha reaching ovaries, is insufficient to begin luteolysis. In the inflamed uterus, the elevation of PGE2 and PGI2 synthesis takes place. Both prostaglandins cause smooth uterine muscles relaxation and the dilatation of blood and lymph vessels in this organ. In these conditions, the blood and lymph outflow from the uterus is several times slower than in the control animals. The secretion of P4 and E2 from CLP, in comparison with control animals, is significantly lower. Decreased P4 concentration during the luteal phase of the estrous cycle, and E2 in the initiation of the luteolysis period, may cause the insufficient preparation of the endometrium for hypophyseal OT activity. Finally, we can assume that the creation of the CLP in the animal ovary is an exceptionally complex and not yet fully understood process.
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PMID:Immuno-endocrine mechanisms connected with the creation of corpora lutea persistent in animal ovaries. 1618 May 88

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