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)

Bovine luteal cells from Days 4, 8, 14 and 18 of the estrous cycle were incubated for 2 h (1 x 10(5) cells/ml) in serum-free media with one or a combination of treatments [control (no hormone), prostaglandin F2 alpha (PGF), oxytocin (OT), estradiol-17 beta (E) or luteinizing hormone (LH)]. Luteal cell conditioned media were then assayed by RIA for progesterone (P), PGF, and OT. Basal secretion of PGF on Days 4, 8, 14 and 18 was 173.8 +/- 66.2, 111.1 +/- 37.8, 57.7 +/- 15.4 and 124.3 +/- 29.9 pg/ml, respectively. Basal release of OT and P was greater on Day 4 (P less than 0.01) than on Day 8, 14 and 18 (OT: 17.5 +/- 2.6 versus 5.6 +/- 0.7, 6.0 +/- 1.4 and 3.1 +/- 0.4 pg/ml; P: 138.9 +/- 19.5 versus 23.2 +/- 7.5, 35.4 +/- 6.5 and 43.6 +/- 8.1 ng/ml, respectively). Oxytocin increased (P less than 0.01) PGF release by luteal cells compared with control cultures irrespective of day of estrous cycle. Estradiol-17 beta stimulated (P less than 0.05) PGF secretion on Days 8, 14 and 18, and LH increased (P less than 0.01) PGF production only on Day 14. Prostaglandin F2 alpha, E and LH had no effect on OT release by luteal cells from any day. Luteinizing hormone alone or in combination with PGF, OT or E increased (P less than 0.01) P secretion by cells from Days 8, 14 and 18. However on Day 8, a combination of PGF + OT and PGF + E decreased (P less than 0.05) LH-stimulated P secretion. These data demonstrate that OT stimulates PGF secretion by bovine luteal cells in vitro. In addition, LH and E also stimulate PGF release but effects may vary with stage of estrous cycle.
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PMID:Prostaglandin F2 alpha, oxytocin and progesterone secretion by bovine luteal cells at several stages of luteal development: effects of oxytocin, luteinizing hormone, prostaglandin F2 alpha and estradiol-17 beta. 278 Oct 46

Both myometrial oxytocin and alpha 2-adrenergic receptors are induced by estrogen. To compare the regulation of these two receptor populations by progesterone, we measured myometrial receptor concentration in ovariectomized steroid-treated and in pregnant rabbits. To control for the effects of estrogen withdrawal, we used concomitant rather than sequential presentation of estrogen and progesterone in ovariectomized rabbits. Estradiol increased both myometrial oxytocin and alpha 2-adrenergic receptor concentrations in ovariectomized rabbits after 8 days of treatment. Simultaneous progesterone administration during the last 4 days of estradiol treatment reversed the induction of oxytocin, but not alpha 2-adrenergic, receptors. Similarly, administration of the antiprogestin RU 38486 to pregnant rabbits on day 27 of gestation resulted in premature delivery and evoked an increase in myometrial oxytocin receptor concentration mimicking that observed at term (day 31). However, RU 38486 did not significantly affect alpha 2-adrenergic receptor concentration. Our data provide further support for involvement of oxytocin receptors in parturition, but do not indicate a comparable function for myometrial alpha 2-adrenergic receptors.
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PMID:Rabbit myometrial oxytocin and alpha 2-adrenergic receptors are increased by estrogen but are differentially regulated by progesterone. 302 88

Previous studies have provided evidence for a discrete localization of two types of vasopressin (AVP)-labeled binding sites in the rat brain, i.e., regions labeled preferentially with AVP (putative AVP receptors) and regions labeled with AVP as well as oxytocin (OT). The latter binding sites are considered here as putative OT receptors. In the present study the effect of estradiol on the number of these putative receptor sites for OT and AVP was investigated in rat brain after daily subcutaneous administration of the steroid (10 micrograms/100 g body weight) to ovariectomized rats. Specific binding of [3H]-OT and [3H]-AVP was determined after in vitro incubation of frozen brain sections, autoradiography and quantitation of the images with computer-assisted densitometry. Estradiol increased the number of OT receptors at least 4-fold in the ventromedial nucleus of the hypothalamus, regions of the olfactory tubercle, the nucleus accumbens and occasionally in the organum vasculosum laminae terminalis. A smaller increase (two-fold) was noted in the central amygdala, while a tendency to a decrease in OT receptor number was noted in the olfactory nucleus and the ventral subiculum. Estradiol treatment permitted an estimation of binding constants of [3H]-OT-binding to a membrane fraction of microdissected ventromedial hypothalamic region (Kd: 1.3 nM, Bmax: 19.9 fmol/mg protein). The number of putative AVP receptors in the lateral septum and in the nucleus tractus solitarii was not affected by estradiol. In conclusion, the OT receptor system is subject to modulation by estradiol in some discrete brain regions, but not in others.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Estradiol modulates density of putative 'oxytocin receptors' in discrete rat brain regions. 302 14

Twenty ovariectomized ewes were used in an experiment designed to examine the interaction of progesterone, estradiol, and oxytocin in the regulation of uterine secretion of prostaglandin F2 alpha (PGF2 alpha). All ewes underwent a steroid pretreatment that mimicked the changes in progesterone and estradiol which occur during the six days immediately prior to estrus. After pretreatment, ewes were randomly assigned to 1 of 4 treatment groups: 1) control (n = 4); 2) estradiol-17 beta (n = 6); 3) progesterone (n = 4); and 4) progesterone and estradiol-17 beta (n = 6). Progesterone was injected twice daily for 15 days. The dose of progesterone varied with day postestrus in a manner designed to simulate endogenous luteal secretion of progesterone. Estradiol-17 beta was administered in s.c. Silastic implants. The implants maintained circulating concentrations of estradiol at 3 pg/ml. On Days 5, 10, and 15 of treatment, ewes were injected with oxytocin (10 IU in 1.0 ml saline, i.v.). Jugular venous blood samples were collected beginning one-half hour prior to and continuing for 2 hours post-oxytocin injection for quantification of 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM). No changes in concentration of PGFM following injection of oxytocin were observed on Day 5 or 10 in any treatment group. Concentrations of PGFM increased following injection of oxytocin on Day 15 only in groups receiving progesterone. Both the area under the PGFM response curve (p = 0.08) and peak response (p = 0.06) were greater in ewes treated with progesterone and estradiol-17 beta than in those receiving progesterone alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of progesterone and estradiol-17 beta on uterine secretion of prostaglandin F2 alpha in response to oxytocin in ovariectomized ewes. 316 88

This article reviews current understanding of the physiological control of maternal behaviour in parturient ewes. Estradiol is an important endocrine factor which stimulates maternal responsiveness, both in nonpregnant and in parturient ewes. However, its action depends on previous maternal experience, and other factors are also necessary for the rapid manifestation of maternal behaviour. Olfactory cues play a major role in the normal development of the mother-young relationship. Genital stimulation (GS) is a key factor influencing various aspects of maternal responsiveness in sheep. GS acts in synergy with peripheral hormones to induce the rapid onset of licking and immediate acceptance of a neonate at the udder in nonpregnant ewes. It also influences the attraction of amniotic fluid at parturition and reduces aggressive behaviour towards lambs. Deprivation of GS by peridural anesthesia disturbs maternal behaviour in parturient ewes, especially in primiparae. And, additional GS in postparturient ewes allows the formation of a new bond with an alien neonate in mothers which had already established a selective relationship with their own lambs. Some of these positive effects of GS are mediated through modifications of olfactory function (attraction of amniotic fluid, establishment of a selective bond), whereas this may not be the case for other effects (stimulation of licking, reduction of aggressive behaviour). Studies of the neural mechanisms involved will be necessary to specify the modes of action of GS. The first results suggest GS may act in at least two ways at the level of the brain. Stimulation of maternal behaviour could depend on the liberation of oxytocin within the brain, since intracerebroventricular injections of this hormone facilitate maternal responses. Also, GS can influence olfactory function through the activation of afferent noradrenergic pathways in the olfactory bulbs. Further studies need to be developed to specify the relationships between the various structures involved as well as the level at which estradiol exerts its facilitatory action.
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PMID:Genital, olfactory, and endocrine interactions in the development of maternal behaviour in the parturient ewe. 328 20

Spontaneous and drug-induced uterine motility (UM) was recorded in 5 nonanesthetized bitches for 2 to 4 days. Catheter-tip pressure transducers were surgically implanted in 1 uterine horn, tunneled subcutaneously to exit from the skin over the dorsal lumbar area, and protected by a bandage. On the day after implantation, spontaneous UM was recorded in the awake bitch. Effects of IV prostaglandin (PG) F2 alpha (5 micrograms/kg of body weight) and oxytocin (0.05 USP U/kg) and IM PGF2 alpha (25 micrograms/kg) were measured. Estradiol (1 to 25 micrograms/kg) was administered and the study was repeated 24 hours later. In awake bitches, spontaneous UM was 190% greater than UM in anesthetized bitches. Uterine motility was increased by more than 100% after IV PGF2 alpha or oxytocin and by 52% after IM PGF2 alpha. Estradiol abolished spontaneous UM, but did not affect drug-induced responses. Seemingly, spontaneous and drug-induced UM can be documented in the nonanesthetized bitch.
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PMID:Recording uterine motility in the nonanesthetized bitch. 377 47

Activity of 40 single antidromically identified supraoptic neurons was recorded and evaluated in response to a combination of tactile, vulvar massage, vaginal distension, and slow intrajugular 1.2 M sodium chloride infusion in unanesthetized, randomly hydrated ewes. Estradiol-implanted Southdown ewes were prepared according to techniques described by Jennings et al. Only 4 spontaneous firing patterns were observed in the supraoptic nuclei. Analysis of evoked activity indicated that each stimulus evoked alterations in mean firing rates or increased numbers of short interspike intervals in some cells. The resultant activity of units to sequential vulvar massage and 1.2 M sodium chloride infusion suggests a possibility of separate mechanisms of release of oxytocin and vasopressin.
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PMID:Effects of intrajugular hypertonic saline, vaginal distension and vulvar massage on activity of supraoptic neuroendocrine cells. 397 Nov 61

Fertilization failure, mostly due to absence of sperm in the oviducts, is a major cause of reproductive inefficiency of farm animals. Sperm may be transported to the oviducts of cattle and sheep within a few minutes after mating or insemination, but these sperm probably fertilize few ova. Slower transport, with establishment of sperm populations in each segment of the reproductive tract, requires a few to several hours. In swine, sperm capable of fertilizing ova reach the oviducts in less than 1 h. Smooth muscle contractions of the reproductive tract, ciliary beats, fluid currents, and flagellar activity of sperm are primary mechanisms of sperm transport. Sperm become hyperactive in the oviducts in association with capacitation. Most sperm in an inseminate drain from the female reproductive tract within a few minutes or hours after insemination; remaining sperm are removed from the tract by slower drainage or phagocytosis. Sperm survival and transport in estrous ewes is reduced drastically by pastures with high estrogen content and by regulating estrus with progestogen or prostaglandin F2 alpha. The cervix is the initial site of inhibition of sperm transport in ewes, and endocrine imbalances probably are the basis of inhibition. Sperm transport problems generally are associated with immobilization and death of sperm in the uterus and anterior segments of the cervix within 2 h after mating. After gilts are inseminated with frozen-thawed semen, relatively few sperm are retained in the reproductive tract, apparently accounting for lowered fertilization rates. Sperm transport has been improved by adding to semen or administering to females such compounds as prostaglandin F2 alpha, oxytocin, estradiol, phenylephrine, or ergonovine. Estradiol, prostaglandin F2 alpha, phenylephrine, and ergonovine administered to rabbits at insemination each increased fertilization rates.
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PMID:Sperm survival and transport in the female reproductive tract. 636 94

Normal human endometrium (classified by histology and date after last menstrual period) was cultured for 72h, and the output of prostaglandin F2 alpha and 6-oxo-prostaglandin F1 alpha detected by radioimmunoassay. Hormones/stimuli were added to the culture during the second day of culture for 5h and 19h periods. The output of prostaglandin F2 alpha from cultured endometrium was significantly higher (p less than 0.05) at the beginning (d4-8) and end (d25-30) of the menstrual cycle, compared to mid-cycle (d13-24) endometrium. Significantly more prostaglandin F2 alpha was released from proliferative than from secretory phase endometrium (p less than 0.02). Prostaglandin F2 alpha release was rapidly stimulated by sodium arachidonate (20-300 micrograms/ml), and by calcium ionophore A23187 (5 micrograms/ml) at an extracellular calcium ion concentration of 1.8mM. The ionophore stimulation was greater in mid-cycle endometrium than in endometrium from the beginning or the end of the menstrual cycle. Estradiol-17 beta (10 ng/ml) gradually increased the output of prostaglandin F2 alpha from secretory phase endometrium, and this stimulation was observed in the post-incubation period after hormone had been removed from the incubation medium. Oxytocin (1 X 10(-5) U/ml caused a more rapid stimulation of prostaglandin F2 alpha output from secretory phase tissue (p less than 0.05 during the first 5h incubation period with hormone). Oxytocin (1 X 10(-5) U/ml) and estradiol (10ng/ml) together significantly stimulated prostaglandin F2 alpha production by proliferative as well as secretory phase endometria. A high dose of hydrocortisone (100 micrograms/ml) inhibited the output of prostaglandin F2 alpha from proliferative and secretory phase endometrium and also from ionophore-stimulated endometrium. However, this dose of hydrocortisone did not inhibit the synthesis of prostaglandin F2 alpha from exogenous arachidonic acid, or the estradiol-induced increase in prostaglandin F2 alpha production. Co-culture of endometrium with myometrium did not modify the output of prostaglandin F2 alpha or of 6-oxo-prostaglandin F1 alpha from cultured tissues. These experiments suggest that arachidonic acid supply to the cyclooxygenase enzyme may vary during the menstrual cycle; and indicate a gradual increase in prostaglandin synthesising capacity in response to estrogen, more rapid control via oxytocin, and an interaction between estrogen and oxytocin to modulate prostaglandin F2 alpha synthesis in human endometrium.
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PMID:The effect of oxytocin, estrogen, calcium ionophore A23187 and hydrocortisone on prostaglandin F2 alpha and 6-oxo-prostaglandin F1 alpha production by cultured human endometrial and myometrial explants. 642 64

Agents influencing the output of prostaglandin F2 alpha (PGF2 alpha) from non-pregnant endometrium were investigated by in vitro incubation, for 5 and 19h, using mid-cycle (day 7), end of cycle (day 15), or ovariectomised guinea-pigs. Estradiol 17-beta (10 micrograms/ml) stimulated PGF2 alpha output 24h after incubation with endometrium (p less than 0.05). This stimulation was greater at mid-cycle. Progesterone (50 ng/ml) inhibited output of PGF2 alpha (p less than 0.05) in mid-cycle, end of cycle and ovariectomised guinea-pig cultures. Oxytocin (1 X 10(-5) u/ml) stimulated the output of PGF2 alpha at the end of the cycle, but not at mid-cycle. However, in the presence of estradiol 17-beta (10 micrograms/ml), oxytocin stimulation of mid-cycle PGF2 alpha output was observed. The calcium ionophore A23187 (5 micrograms/ml) stimulated PGF2 alpha synthesis from mid-cycle and end-of-cycle endometrium, and this stimulation resembled that caused by arachidonic acid (100 micrograms/ml), suggesting an action via substrate mobilisation. Co-culture of endometrium and myometrium did not influence endometrial PGF2 alpha or myometrial 6-oxo-PGF2 output. It is suggested that the steroid hormones act as coarse modulators of endometrial PGF2 alpha output, but more rapid changes may be achieved by oxytocin and agents that mobilise substrate supply, possibly via calcium ion fluctuations.
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PMID:Control of endometrial prostaglandin output in vitro during the estrous cycle of the guinea-pig: influence of estradiol 17-beta, progesterone, oxytocin and calcium ionophore A23187. 681 62


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