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)

Three experiments were conducted to examine inositol phosphate (IP) turnover in response to treatments applied in vitro to endometrium from cyclic (CYC), pregnant (PREG) and estradiol-induced pseudopregnant (PSP) gilts. In Exp. 1, treatments (in 25 microliters .1 M NaHCO3) were 1) control (NaHCO3), 2) 125 ng oxytocin, 3) .25 micrograms prolactin, 4) 2.5 micrograms prolactin and 5) 5 micrograms pig conceptus secretory proteins (pCSP). Basal IP turnover on d 14 (estrus = d 0) for CYC was 3.9 to 5.0-fold greater than for PREG gilts and .6 to 1.1-fold greater than for PSP gilts (P less than .05). Oxytocin increased IP turnover 23 to 42% in CYC gilts (P less than .05), but not in PREG or PSP gilts. The treatment x reproductive status interaction (P less than .05) indicated that pCSP increased IP turnover 74 to 140% in PREG gilts but decreased it 18 to 22% in CYC and 17 to 50% in PSP gilts. In Exp. 2, treatments were applied in a 2 x 2 x 2 arrangement: 1) 0 or 125 ng oxytocin; 2) 0 or 2.5 micrograms prolactin and 3) 0 or 5 micrograms pCSP. Basal IP turnover on d 14 was 3.3 to 5.4-fold greater (P less than .05) in CYC than in PSP gilts and was affected by interaction (P less than .05) of pCSP and prolactin. Inositol phosphate turnover was increased by prolactin (12 to 22%) and by pCSP (7 to 34%) but, when combined, the stimulatory effects of each were eliminated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endometrial inositol phosphate turnover in pigs is reduced during pregnancy and estradiol-induced pseudopregnancy. 228 69

1. Membrane currents were recorded from voltage clamped Xenopus laevis oocytes, still surrounded by follicular cells, theca and enveloping inner ovarian epithelia (ovarian follicles). 2. Superfusing follicles with frog Ringer solution containing E-series prostaglandins (PGE1 or PGE2) or oxytocin (0.5-2 microM) generated slow membrane currents arising from an increase in membrane conductance to K+. 3. Follicles taken from different frogs varied greatly in responsiveness to PGE and oxytocin. For example, enclosed oocytes with good sensitivity to prostaglandins responded to 1 nM-PGE, whereas follicles from some frogs failed to respond at 5 microM. 4. Oocytes with good responsiveness to PGE also produced K+ currents to PGA1, PGA2, PGB1, 11-deoxy-PGE1 and 11-beta-PGE2, whereas PGF2 alpha, PGI2, PGD2 and 8-iso-PGE1 generally failed to elicit membrane currents. 5. Responses to PGE and oxytocin were mimicked by the adenylate cyclase activator forskolin or by intraoocyte pressure injection of cyclic nucleotides. Responses were potentiated by the phosphodiesterase inhibitors theophylline and 3-isobutyl-1-methylxanthine (IBMX). In IBMX (0.5 mM), human atrial natriuretic factor (ANF) (10-60 nM) elicited a similar K+ conductance. This all implied that cyclic nucleotides played a role in the receptor-channel coupling mechanism of these responses. 6. Defolliculating oocytes effectively abolished responses to prostaglandins, oxytocin and ANF, suggesting that the currents arise in follicular cells. 7. The responses of PGE, oxytocin and ANF thus resembled currents elicited by catecholamines, adenosine, gonadotrophins and vasoactive intestinal peptide (VIP). However, PGE, oxytocin and ANF responses were not blocked by catecholaminergic or purinergic antagonists. Moreover, when comparing follicles isolated from different frogs, the sensitivity to PGE and oxytocin varied independently of that to gonadotrophin or VIP. These experiments suggest that Xenopus ovarian follicles contain specific and distinct receptors for PGE, oxytocin and ANF. 8. Acetylcholine attenuated the cyclic nucleotide-mediated K+ responses, including currents elicited by PGE, oxytocin and ANF. Attenuation was not dependent on, or mimicked by, activation of the inositol phosphate-diacylglycerol messenger pathways located in the oocyte itself, nor was it appreciably blocked by loading follicle-enclosed oocytes with 0.1-1.5 mM-EGTA.
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PMID:Membrane currents elicited by prostaglandins, atrial natriuretic factor and oxytocin in follicle-enclosed Xenopus oocytes. 248 34

Incubation of isolated rat hepatocytes with oxytocin produces a time- and dose-dependent inactivation of glycogen synthase. Such inactivation is associated with an increase in the phosphorylation state of the 88 kDa subunit of the enzyme, as observed after electrophoretic analysis of the 32P-labelled enzyme isolated by immunoprecipitation from cells incubated with [32P]phosphate. CNBr cleavage of the immunoprecipitated glycogen synthase showed that multiple sites were phosphorylated after exposure of the cells to the hormone. The effect of oxytocin on hepatocyte glycogen synthase activity was not observed in the absence of extracellular Ca2+. Inactivation of glycogen synthase by oxytocin was partially abolished in the presence of insulin. These results indicate that the effects of oxytocin on glycogen synthase from rat hepatocytes are similar to those observed for other Ca2+-mediated glycogenolytic hormones, such as vasopressin.
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PMID:Oxytocin inactivates and phosphorylates rat hepatocyte glycogen synthase. 250 22

Binding of [3H]arginine vasopressin (AVP) and [3H]oxytocin to primary monolayer cultures of bovine adrenal chromaffin cells was time-dependent, and the binding sites for each peptide were specific and saturable. Studies with the V1 AVP antagonist d(CH2)5Tyr(Me)2-AVP, the V2 agonist 1-deamino-8-D-AVP and the V2 antagonist d(CH2)5D-Leu2,Val4-AVP indicated that the AVP receptor was V1 in specificity. Scatchard plots showed that each ligand interacted with a single high-affinity, low-capacity binding site: oxytocin dissociation constant (Kd) 0.29 +/- 0.02 nmol/l, maximum binding capacity (Bmax) 7.6 +/- 0.2 fmol/10(6) cells (or 4500 +/- 102 sites/cell) (n = 3); AVP Kd 0.09 +/- 0.02 nmol/l, Bmax 5.1 +/- 0.63 fmol/10(6) cells (or 3050 +/- 318 sites/cell) (n = 3). Although forskolin in concentrations from 1 nmol/l to 1 mmol/l stimulated cyclic AMP (cAMP) production in isolated chromaffin cells, this did not result in detectable catecholamine release. Neither AVP nor oxytocin in concentrations between 10 pmol/l and 10 mumols/l stimulated cAMP production in these cells. Vasopressin in concentrations as low as 10 pmol/l stimulated a sixfold increase in total inositol phosphates; the dose-response curve was triphasic. Oxytocin had little effect on total inositol phosphate accumulation at low concentrations, but concentrations above micromolar stimulated total inositol phosphate production approximately fourfold. There was no measurable release of catecholamines in response to either peptide. The physiological consequences of these AVP-induced changes in inositol phosphate concentrations remain to be elucidated.
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PMID:The interaction of arginine vasopressin and oxytocin with bovine adrenal medulla cells. 254 Dec 18

The effects of the uterine relaxants relaxin and isoproterenol on intracellular free calcium and inositol phosphate formation were investigated in rat myometrium. Preincubation of fura-2-loaded myometrial cell suspensions with relaxin and isoproterenol inhibited the oxytocin-induced stimulation of intracellular free calcium, with EC50 values of 0.02 and 1.0 microM, respectively. Pretreatment of cells with pertussis toxin or replacement of extracellular calcium with 2 mM EGTA inhibited the oxytocin-induced increase in intracellular calcium by 47% and 50%, respectively, but did not inhibit the action of relaxin. (Bu)2cAMP and forskolin also inhibited the effect of oxytocin on intracellular calcium. In uterine strips prelabeled with [3H]inositol, oxytocin stimulated a dose-dependent accumulation of inositol monophosphate, inositol bisphosphate, and inositol trisphosphate, with and EC50 of 0.38 microM, and pertussis toxin inhibited this effect. Relaxin, isoproterenol, chlorophenylthio-cAMP, and forskolin inhibited the oxytocin-stimulated formation of inositol monophosphate, inositol bisphosphate, and inositol trisphosphate. The effect of relaxin on inositol trisphosphate formation was dose dependent, with an EC50 of 0.1 microM. Relaxin and isoproterenol also inhibited inositol phosphate formation in myometrial cells. These data demonstrate the attenuation of contractant-induced elevation in myometrial intracellular calcium and phosphoinositide turnover by uterine relaxants and suggest that these actions may be related. In addition, they provide additional evidence that cAMP-mediated mechanisms may be involved in mediating uterine relaxation.
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PMID:Antagonism of contractants and relaxants at the level of intracellular calcium and phosphoinositide turnover in the rat uterus. 254 7

The addition of oxytocin to minces of rat mammary gland preincubated with (3H)myo-inositol stimulated the formation of inositol phosphate (IP) in both lactating and regressed glands. Stimulation was about 4 times greater in regressed tissue, consistent with an oxytocin effect on myoepithelial cells, which are enriched relative to epithelial cells during regression. The stimulation of IP formation was agonist specific, as shown with several oxytocin analogs. Arginine vasopressin (AVP), however, was more than twice as potent as oxytocin in stimulating IP formation in regressed tissue. Both V1- and V2-selective AVP receptor antagonists inhibited the stimulation of IP formation by oxytocin. The V1-selective antagonist was about 10 times more inhibitory than the V2-selective antagonist. [3H]AVP was bound to plasma membranes from the mammary gland of the lactating rat with an apparent Kd of about 0.7 nM and Bmax of 54.6 fmol/mg protein. These values were comparable with those found for AVP receptors of kidney plasma membranes. Our results suggest that the stimulation of IP formation in rat mammary gland by oxytocin occurs through occupancy of AVP, and not oxytocin, receptor sites. A second aspect of these studies was to determine if a recently developed iodinated antagonist of oxytocin-induced uterine contractions could be used as a specific probe for oxytocin receptors in the rat mammary gland. Under steady state conditions, [125I]d(CH2)5(1)[Tyr(Me)2,Thr4,Tyr-NH2(9)]OVT was bound to a single class of independent binding sites in mammary gland plasma membrane from lactating rats with an apparent Kd of 65 pM and Bmax of 225 fmol/mg protein. Noniodinated antagonist had an affinity about 150 times less than the monoiodinated form. The affinity of binding sites for AVP was 10 times greater than the noniodinated antagonist and 2.4 times greater than oxytocin. In view of the presence of AVP receptors in mammary tissue, these findings suggested that the iodinated antagonist binds to AVP receptors. However, comparison of the binding of iodinated antagonist to plasma membranes from the lactating mammary gland with kidney medulla and liver, target sites for AVP, showed that binding was specific for the mammary gland and hence oxytocin receptors. The concentration of oxytocin receptors in mammary gland, as determined by [125I]d(CH2)5(1)[Tyr(Me)2,Thr4,Tyr-NH2(9)]OVT binding, was 4 times greater than the concentration of high-affinity AVP receptors, as determined by [3H]AVP binding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasopressin and oxytocin receptors on plasma membranes from rat mammary gland. Demonstration of vasopressin receptors by stimulation of inositol phosphate formation, and oxytocin receptors by binding of a specific 125I-labeled oxytocin antagonist, d(CH2)5(1)[Tyr(Me)2, Thr4,Tyr-NH2(9)]OVT. 254 75

The effects of porcine relaxin (3000 units/mg) on oxytocin (OT) and progesterone secretion were studied in beef heifers on Day 274 (10 days before expected parturition). Heifers (n = 11) were randomly assigned to three treatments: relaxin iv infusions combined with im injection (RLX-INF, 9000 units), relaxin im injection (RLX-im, 6000 units), and phosphate-buffered saline-treated controls (PBS). RLX-INF heifers received infusions of PBS and 1000 units of relaxin for 165 min, followed by 2000 units of relaxin im and finally 2000 units of relaxin infusion followed by 4000 units of relaxin im. Endogenous relaxin (immunoreactive) in the PBS-treated group was 0.2-0.9 ng/ml peripheral plasma. For the RLX-im group, peak relaxin was 81 +/- 12 ng/ml (+/- SE) at 45 min after treatment. There were two peaks of relaxin, 18 +/- 5.3 ng/ml and 74 +/- 7.5 ng/ml, 3.5-4.5 hr apart in the RLX-INF group. Significant peak releases of OT were evident in the relaxin-treated heifers. For the RLX-im group, an OT peak (42 +/- 16 pg/ml) occurred within 30 min after relaxin treatment. For the RLX-INF heifers, 2000 and 4000 units of relaxin were associated with major peaks of 14 +/- 0.5 and 43 +/- 1.7 pg/ml OT, respectively. Basal OT plasma levels in the PBS group were 2.5-3.1 pg/ml. Mean plasma progesterone for all heifers was 6.2 +/- 2.11 ng/ml before treatment. There was a significant decrease in progesterone (-2.5 ng/ml) in the RLX-im group within 60 min after relaxin treatment and 45 min after peak OT secretion. The maximum decrease in progesterone (-3.2 +/- 0.68 ng/ml) occurred 135 min after treatment in the RLX-im group. In the RLX-INF group, 2000 units of relaxin infusion combined with 4000 units of relaxin im significantly decreased progesterone (-3.2 +/- 1.59 ng/ml) in peripheral plasma. These results clearly indicate that relaxin causes an acute peak release of oxytocin within 30 min, followed by a marked decrease in plasma progesterone concentration in late-pregnancy cattle.
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PMID:Relaxin regulates oxytocin secretion in late-pregnant beef heifers. 272 77

The presence of oxytocin and mesotocin in the hypothalamus of two Australian marsupials, the bandicoot (Isoodon macrourus) and the brushtail possum (Trichosurus vulpecula), was examined by immunocytochemistry. Tissue was fixed in paraformaldehyde in phosphate buffer and immunoreactive cells were detected using highly specific rabbit antioxytocin and sheep anti-mesotocin as primary antisera. Immunoreactive oxytocin cells were demonstrated in the paraventricular and supraoptic nuclei of bandicoot and possum hypothalami, with greater density being observed in paraventricular nuclei. Immunoreactive mesotocin cells were also found in both hypothalamic nuclei of the possum but not of the bandicoot. The same cells appeared to stain for both peptides.
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PMID:Immunocytochemical location of oxytocin and mesotocin within the hypothalamus of two Australian marsupials, the bandicoot Isoodon macrourus and the brushtail possum Trichosurus vulpecula. 276 13

To investigate the bioenergetics of uterine muscles in vivo, we examined the energy state of mouse preterm uterus by means of magnetic resonance spectroscopy. Full-term mouse uterus contained ATP, PCr, phospho-di and mono ester (PDE and PME) and inorganic phosphate (Pi). The oxytocin-induced uterine muscle contraction peaks level and positions changed. Multiple peak analysis indicated a muscle contraction induced increase in the Pi concentration and decrease in the PCr concentration. The peak position of Pi was shifted in the contractive state also, indicating that the intracellular pH was lower than in the non-contractive state and this low pH level was recovered within several minutes. There was no change in the AMP peak height in the contractive and non-contractive states. These data indicated that the energetics of mouse uterine muscle was maintained by the ATP-PCr system and acidosis of muscle was recovered within several minutes at rest. The constant AMP peak levels may indicate that phosphorylase is not regulated by AMP, but the phosphorylated phosphorylase kinase and pH levels in the contractive and non-contractive states also may indicate that phosphorylase kinase is not regulated by proteolysis or by the intracellular pH level but by the elevated intracellular calcium ion and calmodulin system.
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PMID:[The study of bioenergetics of mouse pregnant uterine muscle by magnetic resonance spectroscopy (MRS)]. 276 62

Vasopressin and oxytocin both stimulated inositol phosphate accumulation in isolated uterine decidua cells. Pretreatment of cells with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) prevented this agonist-induced phosphoinositide hydrolysis. TPA (0.1 microM) alone had no effect on basal inositol phosphate accumulation, but stimulated phosphoinositide deacylation, as indicated by a 2-fold increase in lysophosphatidylinositol and glycerophosphoinositol. TPA also stimulated a dose-related release of arachidonic acid from decidua-cell phospholipid [phosphatidylcholine (PC) much greater than phosphatidylinositol (PI) greater than phosphatidylethanolamine]. The phorbol ester 4 beta-phorbol 12,13-diacetate (PDA) at 0.1 microM had no effect on arachidonic acid mobilization. The TPA-stimulated increase in arachidonic acid release was apparent by 2 1/2 min (116% of control), maximal after 20 min (283% of control), and remained around this value (306% of control) after 120 min incubation. TPA also stimulated significant increases in 1,2-diacylglycerol and monoacylglycerol production at 20 and 120 min. Although the temporal increases in arachidonic acid and monoacylglycerol accumulation in the presence of TPA continued up to 120 min, that of 1,2-diacylglycerol declined after 20 min. In decidua cells prelabelled with [3H]choline, TPA also stimulated a significant decrease in radiolabelled PC after 20 min, which was accompanied by an increased release of water-soluble metabolites into the medium. Most of the radioactivity in the extracellular pool was associated with choline, whereas the main cellular water-soluble metabolite was phosphorylcholine. TPA stimulated extracellular choline accumulation to 183% and 351% of basal release after 5 and 20 min respectively and cellular phosphorylcholine production to 136% of basal values after 20 min. These results are consistent with a model in which protein kinase C activation by TPA leads to arachidonic acid mobilization from decidua-cell phospholipid by a mechanism involving phospholipase A-mediated PI hydrolysis and phospholipase C-mediated PC hydrolysis, coupled with further hydrolysis of the 1,2-diacylglycerol product.
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PMID:Stimulation of phospholipid hydrolysis and arachidonic acid mobilization in human uterine decidua cells by phorbol ester. 282 48


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