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

Expanded use of artificial insemination in the beef cattle industry depends on successful application of treatments designed to synchronize estrus. Regulation of estrous cycles is associated with control of the corpus luteum (CL), whose life span and secretory activity are subject to trophic and lytic mechanisms. The advantages of melengestrol acetate (MGA) in estrous synchronization incorporate ease of administration, lower cost relative to other estrous synchronization products, and potential for use to induce estrus in prepubertal heifers. Treatments first designed to synchronize estrous cycles of normally cycling heifers by feeding MGA were imposed daily for 14 to 18 d at levels of .5 to 1 mg. The minimal daily effective dose required to inhibit ovulation was .42 mg. Longer feeding periods of MGA were associated with low fertility at the first synchronized estrus, but at the second estrus, conception was normal. Low fertility at the synchronized estrus resulted in development of alternative treatment practices, which combined feeding of MGA with injections or implants of estradiol-17 beta, estradiol cypionate, luteinizing hormone, human chorionic gonadotropin, pregnant mare serum gonadotropin, or oxytocin. Estrus was synchronized after MGA and estradiol-17 beta or estradiol cypionate treatments, but fertility was low. Short-term feeding of MGA (5 to 7 d) combined with prostaglandin F2 alpha or its analogs (PGF) on the last day of MGA reduced fertility at the synchronized estrus. The reduced conception at first service occurred in animals that began treatment after d 12 of the estrous cycle. However, feeding MGA for 14 d and then injecting PGF 17 d later avoided problems with reduced conception. Fertility of animals after this treatment was similar to that of contemporaries synchronized with Syncro-Mate-B. However, the length of the treatment period creates a need for increased management and may extend management beyond practical limits. Further research is warranted to address problems associated with reduced fertility after short-term treatment with MGA.
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PMID:Control of the bovine estrous cycle with melengestrol acetate (MGA): a review. 267 33

We have investigated the possibility that the mitochondria-rich (MR) cells participate in sodium and proton transport, when the frog skin epithelium is bathed on its apical side with solutions of low Na+ concentration, by comparing transport rates with morphological observations (MR cell number and MR cell pit surface area). Frogs were adapted to various salinities or the isolated skins were treated with the following hormones, deoxycorticosterone acetate (DOCA), arginine vasotocin (AVT) and oxytocin in order to modify the transport of sodium and hydrogen ions. Adaptation of the frogs (either 3-4 days or 7-10 days) to distilled water, NaCl (50 mmol/l), KCl (50 mmol/l) or Na2SO4 (25 mmol/l) solutions modified the Na+ transport rate and the morphology of the epithelium. The highest Na+ transport rates were found for the animals adapted to the Na+ free solutions and were correlated with an increase in the total MR cell pit surface area (number of MR cells x individual cell pit-surface area). The KCl adaptated group showed the largest increase in sodium and proton transport and also presented a metabolic acidosis as reflected by plasma acidification (pCO2 increase and HCO3- decrease). Proton secretion and sodium absorption were also found to be stimulated by either serosal DOCA addition (10(-6) M) or during acidification of the epithelium by serosally applied CO2. Na+ transport was enhanced by AVT (10(-6) M) or oxytocin (100 mU/ml) when the skin was bathed on its apical side with a high Na+ containing solution (115 mmol/l), whereas these hormones did not exert any effect on Na+ transport when the apical solution was low in Na+ (0.5 mmol/l).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The key role of the mitochondria-rich cell in Na+ and H+ transport across the frog skin epithelium. 278 88

In the present experiments we examined neurohypophyseal hormone secretion in various models of sodium appetite in rats. Basal plasma levels of oxytocin were found to be low in sodium-deficient adrenalectomized rats and in intact animals treated daily with desoxycorticosterone acetate, both of which groups drank large amounts of NaCl solution, whereas basal plasma levels of arginine vasopressin were neither stimulated nor suppressed. Conversely, sodium appetite consistently was inhibited by treatments that stimulated pituitary oxytocin secretion. However, sodium appetite was not inhibited by administration of exogenous oxytocin, nor was it stimulated by administration of an oxytocin receptor antagonist. These and other results suggest that sodium appetite may be inhibited by activity in the supraoptic and/or paraventricular nuclei, the location of the neurons responsible for the synthesis of oxytocin, and can be stimulated only when activity in those neurons is reduced. Whatever the final neural pathway, our data support the hypothesis that the control of sodium appetite is governed by inhibitory as well as excitatory central mechanisms.
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PMID:Central inhibitory control of sodium appetite in rats: correlation with pituitary oxytocin secretion. 282 Apr 37

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

It has been postulated that fetal hormonal signals act upon amnion to trigger labor via prostaglandin (PG) production. Human amnion epithelial cell cultures were established to test the effects of potential activators of the inositol phospholipid-protein kinase-C effector system on intracellular inositol phosphate turnover, intracellular free calcium ([ Ca2+]i), and PGE2 production. Oxytocin provoked 3-, 2.5-, and 4-fold increases in inositol triphosphate, inositol bisphosphate, and inositol monophosphate, respectively. [Ca2+]i, measured with the fluorescent dye fura-2, was stimulated by oxytocin and vasopressin (oxytocin greater than vasopressin) in a dose-dependent manner. The [Ca2+]i transient produced by oxytocin reached a peak in 15 sec, followed by a slow return to baseline over 10 min. Preincubation with phorbol 12-myristate-13 acetate (PMA) markedly blunted the oxytocin-induced transient. No [Ca2+]i transient was seen with leukotrienes, PG, serotonin, angiotensin, or alpha- or beta-adrenergic agents. PGE2 production increased 30- to 50-fold with phospholipase-C and PMA, and 10-fold with the calcium ionophore A23187. Oxytocin and vasopressin produced 10- and 3-fold PGE2 increases, respectively. Increased PGE2 production induced by PMA, oxytocin, and A23187 was first seen after 8 hr of incubation and reached maximal levels at 24 h. Minimal PGE2 stimulation occurred with agents that produced no [Ca2+]i transient. Direct activators of the inositol phospholipid-protein kinase-C system in human amnion induce large increases in PGE2 in human amnion cells. Oxytocin and vasopressin are hormonal activators of this system in these cells, as demonstrated by their effects on inositol phosphate turnover and [Ca2+]i. These hormones also increase PGE2 production and may influence labor by stimulating PGE2 production in amnion through the inositol phospholipid-protein kinase-C system.
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PMID:Oxytocin activates the inositol-phospholipid-protein kinase-C system and stimulates prostaglandin production in human amnion cells. 313 2

Two experiments were conducted to determine if the ability of oxytocin to stimulate release of prostaglandin (PG)F2 alpha from ovine uterine tissue involved activation of phospholipase C (PLC). In the first experiment, 9 ewes were injected with progesterone for 11 d (12 mg/d, im). On days 11 and 12, ewes received an injection of estradiol (100 micrograms, im). Caruncular endometrial tissue was collected on d 13 and incubated in the presence or absence of oxytocin (10(-6) M). Concentrations of PGF2 alpha and its metabolite, 13,14-dihydro-15-keto-PGF2 alpha (PGFM), in culture media were determined by radioimmunoassay. PLC activity was determined by measuring the intracellular accumulation of 3H-inositol phosphates after preincubation with 3H-inositol. Concentrations of PGF2 alpha and total PGF (PGF2 alpha + PGFM) in culture media were greater for explants treated with oxytocin than for controls (p. less than .02, p less than .06, respectively). A similar effect of oxytocin on intracellular concentrations of 3H-inositol phosphates was observed (p less than .01). A second experiment was conducted to determine if agonists of second messengers, produced by activation of PLC, could stimulate release of PGF2 alpha from ovine endometrial tissue. Seven ewes were treated with progesterone and estradiol as in experiment 1. Explants of caruncular tissue from each ewe were incubated with 1) control medium, 2) A23187 (10(-5) M), 3) oxytocin (10(-6) M), 4) phorbol 12-myristate 13-acetate (PMA, 10(-7) M), 5) PMA + A23187 and 6) PMA + oxytocin. Significant stimulatory effects of oxytocin, PMA and A23187 on concentrations of PGF2 alpha and total PGF in culture media were observed (p. less than .05, p less than .1, p less than .1, respectively). In conclusion, oxytocin stimulated release of PGF2 alpha and activity of PLC in explants of ovine endometrial tissue in vitro. Second messengers associated with activation of PLC enhanced release of PGF2 alpha from ovine endometrial tissue.
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PMID:Role of phospholipase C in mediating oxytocin-induced release of prostaglandin F2 alpha from ovine endometrial tissue. 324 71

Neurophysin 1 (a peptide associated with antidiuretic homone, ADH), ADH, and oxytocin were measured in serum or urine of 3 men who took 10 mcg ethinyl estradiol with 5 mg norethisterone acetate twice daily for 6 days and in 3 who took the estrogen only. Neurophysin in plasma was determined by radioimmunoassy, and individually by starch gel electrophoresis, extraction, and assay. Total urine neurophysin was measured by radioimmunoassy. ADH and oxytocin were quantitated by column chromatography and radioimmunoassy. With both steroids, there was no change in neurophysin, ADH, or oxytocin. Ethinyl estradiol alone increased urinary neurophysin from 112.3 to 595 ng/hour (n.s.), oxytocin from 41-132 ng/hour (p less than .005), and ADH from 9.7-57.2 ng/hour (p less than .01). As in pregnant women compared to normal women, estrogen treatment stimulated plasma neurophysin 1 more than neurophysin 2 in these subjects. These results confirm those found in rats.
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PMID:[Interactions between a progestational derivative (norethisterone acetate) and ethinyl estradiol on urinary elimination of neurophysin, ocytocin, and vasopressin and on the blood level of neurophysin I and II in normal human beings]. 460 73

1. The effect of milking goats 1-4 times an hour for 3-12 hr on the yield and composition of milk has been studied in fed and fasted animals at all stages of lactation.2. It was essential to inject oxytocin (50-400 m-u. I.V.) just before each milking to remove all the milk already in the udder and then the yield was similar to that obtained on twice daily milking (105 +/- 2.1 S.E.%). There were no significant differences between goats or between the two glands of one goat, even if one had been denervated by autotransplantation. However, the variation from hour to hour was 1.5 times greater than from day to day.3. The claim of Zaks (1964) and Zaks, Natochin, Sokolova, Tanasichuk & Tverskoy (1965) that milking every 15 min always produces a large rise in milk Na and a fall in K and lactose, which is characteristic of alveolar milk, is not substantiated. In high yielding goats milking gently by hand or with a cannula caused a small change in K only, but vigorous hand milking exacerbated this fall and also caused a fall in lactose and a rise in Na and Cl. Still larger changes were produced by using excessively large doses of oxytocin (2500 m-u.) when there was also a rise in citrate and total nitrogen. Hourly milking in goats fasted for 24 hr had the same effect.4. In fasted goats the milk yield fell to 90% within 8 hr and to 56 +/- 2.1% of the previous level by 24 hr. It remained at this level for a further 10-12 hr on twice daily or on hourly milking. The yields of autotransplanted glands usually fell slightly but significantly more than that of the glands in situ. In most goats mammary blood flow was halved but in all animals there were large falls in mammary uptake of glucose, acetate and amino acids and greatly increased uptake of free fatty acids. There were significant differences between fasted goats on hourly milking.5. It is concluded that, in spite of changes in milk composition, milking hourly can be a useful technique for studying milk secretion. The striking effects of a short fast in a lactating animal are emphasized.
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PMID:The effect of very frequent milking and of oxytocin on the yield and composition of milk in fed and fasted goats. 606 46

1. Experiments have been carried out in lactating goats milked hourly to assess the value of this technique in studies of milk secretion.2. On refeeding 24 hr-fasted goats there was an increase in arterial concentration and mammary uptake of volatile fatty acids within an hour, but little increase in hourly milk and lactose yield until the mammary uptake of glucose had also increased (after 2-3 hr).3. Intravascular infusions of acetate had no effect on milk secretion in 24 hr-fasted goats but glucose infusions increased milk yield by 62 +/- 5% and lactose yield by 87 +/- 12% within 3 hr, with no effect on fat secretion. The addition of acetate or acetate plus amino acids had no more effect than glucose alone.4. The yield of milk and lactose could be reduced within an hour by insulin (2 u./kg I.V.) and this was prevented or reversed by injecting glucose. In one goat, where in spite of a fall in blood sugar, mammary arteriovenous difference and blood flow did not fall, there was little or no fall in milk yield.5. In fasted or insulin treated goats an increase in milk and lactose secretion could be obtained within an hour by infusing glucose into the artery of one gland autotransplanted to the neck, which responded before the control gland in situ, thus showing that the effect of glucose is directly on the mammary tissue.6. In two normally fed goats with a low blood sugar, glucose infusions increased the milk or lactose yield by 30% within 3 hr.7. It is concluded that frequent milking, using minimal doses of oxytocin, is a valid method of studying factors controlling milk secretion and that, in the lactating goat, the availability of glucose to the mammary gland can be a limiting factor for maximum milk secretion.
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PMID:The effect of infusions of glucose, acetate and amino acids on hourly milk yield in fed, fasted and insulin-treated goats. 606 16

In neural lobes of Sprague-Dawley rats fixed with glutaraldehyde but without osmication, toluidine blue staining of semi-thin sections revealed two clear axon types: type I, highly stained, and type II, slightly stained. After uranyl acetate and lead citrate impregnation of adjacent ultrathin sections, electron microscopy showed that type I axons contained electron-dense granules whereas type II axons mostly contained pale granules. When adjacent semi-thin sections were stained with toluidine blue or treated for immunocytochemistry, type I axons were found to react with vasopressin antisera, and type II axons with oxytocin antisera. In neural lobes of Brattleboro rats, only type II axons were observed and contained pale granules. Both in light and electron microscopy, glutaraldehyde fixation without osmication, therefore provided a simple and reliable approach to distinguish between neurohypophyseal axons containing vasopressin and oxytocin, respectively.
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PMID:Light- and electron-microscope differentiation of axons containing vasopressin and oxytocin in the neurohypophyseal lobe of the rat. 616 86


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