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 distribution of vasopressin (VP), oxytocin (OXY) and neurophysins 1 and 2 (N1, N2) has been studied in the median eminence (ME) of normal, heterozygous (HDI) and Brattleboro (DI) rats. Numerous thin periportal VP and N2 fibres exist in the normal and HD1 rats; they have never been observed in the DI rats. N1 and OXY fibres in the external layer of the median eminence are rare. Adrenalectomy increases periportal VP and N2 loading in normal and HDI rats; it does not modify the appearance of the DI median eminence. Dexamethasone prevents external VP and N2 overloading in adrenalectomized rats injected during the whole postoperative period. Injections of vasopressin indicated that it had a negative feedback effect during a short time (3 days) but not during a longer period (7 days). The suprachiasmatic neurons are stained only by anti-VP and anti-N2 antibodies. Their overstaining induced by adrenalectomy disappears with dexamethasone, aldosterone or vasopressin treatment. This central effect of hormones is not necessarily associated with disappearance of overloading in the external layer of the ME. The hypothalamo-infundibular tract carrying VP and N2 is involved in regulatory mechanisms of the corticotrope axis. Its relationships with suprachiasmatic neurons are discussed.
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PMID:Infundibular localization of vasopressin, oxytocin and neurophysins in the rat; its relationships with corticotrope function. 22 Oct 71

Fifty-six patients, chosen by random sampling from a total group of 120 post-term women, received dexamethasone (Decadron, "MSD" 2 mg 3 times a day for 4 days, the other 64 patients acting as controls. The evolution of uterine activity was evaluated using pelvic score (PS) and a modified low dosage oxytocin sensitivyt test (OST) before (T1) and after (T2) the treatment. During the interval from the second to the 6th day inclusive after T1 35 women of the dexamethasone group and 15 of the control group had a spontaneous onset of labour (SO) (0.001 less than P less than 0.01). Five patients in the dexamethasone group with primary rupture of membranes started labour spontaneously within 12 hours after membrane rupture, 7 patients in the control group with primary rupture of membranes received oxytocin as labour did not start within 24 hours. Excluding patients artifically induced, the mean interval from T1 to SO was 6.8 days in the control group and 5.2 days in the dexamethasone group (P less than 0.001). In both groups PS and the sum of Montevideo units (MU) during OST increased from T1 to T2, the increase was significantly greater in the dexamethasone group than in the control group. We found no correlation between the results of OST and the T1--SO interval. Dexamethasone, as used in this study, may promote labour in prolonged human pregnancy. Due to its low potency, it is not a substitute for oxytocin in the induction of labour. The lowered placento-fetal quotient in the dexamethasone group warrants further study of the effects of steroid hormone on placental function.
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PMID:The effect of dexamethasone therapy in prolonged pregnancy. 60 16

Bilateral adrenalectomy (ADX) leads to increased ACTH synthesis and secretion. It is thought that endogenous glucocorticoids exert a feedback mechanism at both pituitary and brain levels. The present study has been performed in order to determine the effect of ADX on the release of hypothalamic neuropeptides with corticotropin-releasing activity (CRA) and if there exists a median eminence site of glucocorticoid action to regulate hypothalamic-pituitary-adrenal (HPA) function. Adrenalectomized and sham-operated male rats were killed at different periods after surgery (2, 5, 7 and 14 days) and trunk blood was collected for ACTH and corticosterone (B) concentrations measurement. Brain (median eminence, ME; and medial basal hypothalamus, MBH) and pituitary (anterior lobe, AP; and neurointermediate lobe, NIL) tissues were dissected in order to evaluate either peptide content or in vitro hormone release. The results indicate that ADX blunted plasma B levels and increased AP ACTH content and secretion in a time-related fashion up to the 14th day. ADX significantly decreased both CRF and CRA contents in the ME at all periods studied; ME arginine-vasopressin (AVP) increased 7 and 14 days after ADX. MBH CRF decreased after ADX, but returned to sham value 2 weeks later; similarly, MBH AVP decreased at all periods after ADX. Removal of endogenous glucocorticoids did not vary neither oxytocin (OXY) content in the ME and MBH nor AVP and OXY contents in the NIL. In our superfusion experiments, we found that ADX increased basal AVP release and did not change spontaneous CRF secretion from ME terminals. Dexamethasone (Dxm, 10 nM) diminished AVP but not CRF output by ME tissues from adrenalectomized rats. A direct relationship was found between ME CRF and 28 mM KCl (hK+)-induced CRF release by MEs from adrenalectomized rats. ME fragments from adrenalectomized rats were hyperresponsive to kH+ stimulation of AVP release. Dxm (10 nM) decreased the hK(+)-evoked CRF and AVP release by MEs from adrenalectomized rats. ADX and dexamethasone treatment did not influence basal and hK(+)-elicited ME OXY release. Additionally, a rapid glucocorticoid inhibitory effect on ACTH secretion by isolated AP cells from both sham and adrenalectomized rats was found, and an in vitro corticotrope hyporesponse to 0.63 nM CRF and 9.25 nM AVP stimulation during several days after ADX.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Changes in the hypothalamo-corticotrope axis after bilateral adrenalectomy: evidence for a median eminence site of glucocorticoid action. 184 20

In this study we examined the effects of 2% saline loading (S), partial restriction of water consumption (R) or a combination of S or R with dexamethasone (DEX) treatment for 14 days on corticotropin releasing factor (CRF)-41 content of the neurointermediate lobe (NIL) and supraoptic nuclei (SON) of male Wistar rats. Arginine vasopressin (AVP) and oxytocin (OXY) contents of the NIL and SON were also assayed as well as plasma corticosterone, ACTH, [Na+] and [Cl-] concentrations. S or R for 14 days resulted in an increase in CRF-41 content and a concomitant drop in AVP and OXY contents of the NIL. Dexamethasone treatment enhanced the effect of S but not of R on NIL CRF-41 content. Dexamethasone treatment abolished the decrease in the AVP content and partially reversed the decrease in the OXY content of the NIL in response to S but not in response to R. No changes were observed in CRF-41, AVP and OXY content of the SON. Unstressed plasma corticosterone concentrations were not changed in S rats but were elevated in R rats; DEX did not prevent this elevation. Plasma ACTH concentrations were low in all groups examined. Plasma [Na+] and [Cl-] increased in response to both S and R. Increases in [Na+] and [Cl-] evoked by S but not R were prevented by DEX treatment. The results show that in the NIL, osmotic stimulation decreases AVP and OXY content, while it increases the CRF-41 content.
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PMID:Osmotic stimulation affects neurohypophysial corticotropin releasing factor-41 content: effect of dexamethasone. 234 90

1. The effects of adrenalectomy (3 weeks) and dexamethasone (3 h) treatment on the release of corticotrophin-releasing factor-41 (CRF-41), arginine vasopressin (AVP), oxytocin (OT), adrenocorticotrophin (ACTH) and corticosterone were studied in adult female Wistar rats. 2. The animals were anaesthetized with sodium pentobarbitone which, as assessed by the effects on the circadian rhythm of plasma ACTH and corticosterone, appeared to be a better anaesthetic than either urethane or alphaxalone for studies on the hypothalamic-pituitary-adrenal system. 3. Adrenalectomy increased the concentrations of ACTH in peripheral plasma and the output of CRF-41 and AVP into hypophysial portal plasma. 4. Dexamethasone administered to adrenalectomized rats significantly reduced the concentration of ACTH in peripheral plasma and the amount of AVP released into portal plasma. However, dexamethasone did not affect the output of CRF-41 into portal blood. 5. The output of OT into portal plasma was unaffected by either adrenalectomy or dexamethasone treatment. 6. Dexamethasone administered to adrenalectomized rats reduced significantly the ACTH response to CRF-41. 7. These results show that the feed-back action of glucocorticoids is mediated by two mechanisms. The increased release of ACTH which follows adrenolectomy [corrected] is produced predominantly by an increased release of both CRF-41 and AVP into hypophysial portal blood. The intermediate negative feed-back of glucocorticoids is produced by a reduction in the output of AVP but not CRF-41 into portal blood and, as well, by a significant reduction in the responsiveness of the anterior pituitary gland to CRF-41.
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PMID:Effects of adrenalectomy and glucocorticoids on the peptides CRF-41, AVP and oxytocin in rat hypophysial portal blood. 284 63

We have previously demonstrated in pregnant sheep that ritodrine infusion for 24 hours reduces myometrial beta-adrenergic receptor density and isoproterenol-stimulated adenylate cyclase activity. These receptor-associated changes were accompanied by an increasing inability of ritodrine to inhibit uterine contractility induced by a bolus of oxytocin. In the present study, we evaluated whether these ritodrine-induced effects could be altered by dexamethasone. Ten pregnant sheep at gestational ages of 92 to 130 days received ritodrine 2 micrograms/kg/min for 24 hours. Five animals also received dexamethasone 10 mg intravascularly twice during the ritodrine infusion. Before and at 4 and 24 hours of ritodrine infusion, the animals were given an identical dose of oxytocin as a bolus, and the area under the uterine pressure-time curve was quantified. Myometrial biopsy specimens were obtained before and after ritodrine infusion. Dexamethasone treatment prevented ritodrine-induced reductions in beta-adrenergic receptor density and isoproterenol-stimulated adenylate cyclase activity. Despite these receptor-associated effects, dexamethasone did not prevent the loss of tocolytic efficacy associated with prolonged ritodrine infusion.
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PMID:Dexamethasone effects on ritodrine-induced changes in myometrial contractility and beta-adrenergic receptor function. 284 80

The survival of adult rat hepatocytes in monolayer culture was studied in the presence of different hormones (neurotensin, oxytocin, thyrotropin releasing hormone, luteinizing hormone releasing hormone, cholecalciferol, bradykinin, substance P, aldosterone, melanocyte stimulating hormone, 3,3',5-triiodo-1-thyronine, corticosterone, human growth hormone, glucagon, insulin, progesterone, testosterone, estradiol, and dexamethasone phosphate) or growth factors (fetal bovine serum). For this purpose trypan blue exclusion, lactate dehydrogenase, and DNA and protein content were measured at 24 and 72 h of culture. 10(-7) M Dexamethasone, a mixture of eight hormones, 10% fetal bovine serum, and a combination of the latter two supplements caused a more than 64% higher DNA content at 72 h when compared to control cultures. A striking agreement of these results with changes of lactate dehydrogenase leakage was observed, whereas trypan blue exclusion gave erratic results. Considerable changes of cell arrangement apparently specific for each supplement were observed by low magnification microscopy. It is concluded that glucocorticoids and fetal bovine serum have an outstanding effect on cell viability and that DNA or protein content or both are reliable indicators of cell viability in amitotic cultures.
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PMID:Influence of hormones and growth factors on viability, DNA, and protein content of adult hepatocytes in primary culture. 405 11

Basal density and estrogen induction of oxytocin binding sites in limbic and hypothalamic structures of the rat brain were investigated by semi-quantitative autoradiography following chronic administration of dexamethasone or progesterone. The selective oxytocin receptor antagonist d(CH2)5[Tyr(Me)2,Thr4,Tyr-NH2(9)] ornithine-vasotocin was used as a ligand for oxytocin binding sites. Estrogen administration increased ligand binding in all sites investigated. Dexamethasone treatment significantly increased ligand binding in the bed nucleus of the stria terminalis, lateral ventral septum and amygdala to an extent which was comparable to that of estradiol alone. In the hypothalamic ventromedial nucleus, dexamethasone significantly decreased basal levels of oxytocin binding. Estrogen administration subsequent to dexamethasone failed to cause a further increase in oxytocin binding in all structures investigated. Chronic progesterone treatment significantly increased basal oxytocin receptor density in the limbic structures, decreased it in the ventromedial nucleus, and prevented estrogen-induced increases in ligand binding in all areas studied with the exception of the medial preoptic area. These findings demonstrate that, in addition to gonadal steroids, glucocorticoids differentially and site-specifically modulate cerebral oxytocin binding sites. The evidence for glucocorticoid and gestagen influences on oxytocin receptors and their inducibility by estrogen may be relevant to the understanding of mechanisms leading to impairment of oxytocin-related behaviours.
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PMID:Oxytocin binding sites in rat limbic and hypothalamic structures: site-specific modulation by adrenal and gonadal steroids. 830 22

Effects of novel environmental stimuli on vasopressin and oxytocin secretion by the pituitary were studied in dehydrated male rats. As the novel environmental stimuli, rats were transferred to an experimental room, placed in a box painted black and given a pure tone auditory stimulus of 2 kHz. Exposure of rats to the novel environmental stimuli for a period of 2 min decreased plasma concentrations of vasopressin and increased plasma levels of adrenocorticotrophic hormone (ACTH) and prolactin, but did not significantly change the plasma level of oxytocin. The stimuli, however, became ineffective for producing the suppressive vasopressin response as the period of exposure was prolonged to more than 5 and up to 30 min, although the prolonged stimuli were still effective for inducing facilitatory ACTH and prolactin responses. After repeated exposures of rats to the environmental stimuli once a day for 5 or 10 days, the stimuli became disabled from producing the suppressive vasopressin response. However, the rats were still capable of responding to the novel stimuli of another kind. All these data suggest that novelty stress suppresses vasopressin secretion but does not change oxytocin secretion. In order to test the possibility that glucocorticoids expectedly secreted by the adrenals in response to the stress might have suppressed vasopressin secretion, a large amount of dexamethasone was administered to the rat before testing. Dexamethasone pretreatment depressed plasma levels of ACTH and vasopressin as reported previously and blocked the facilitatory ACTH response to the novelty stress. However, dexamethasone treatment did not affect the suppressive vasopressin response to the novelty stress.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of novelty stress on vasopressin and oxytocin secretion by the pituitary in the rat. 840 60

The present studies were designed to examine the regulation of leptin release in primary cultures of adipocytes from fed hypothyroid rats incubated with hormones for 24 hours. Leptin release was increased in the presence of dexamethasone, while the decrease in leptin mRNA content over a 24-hour incubation was reduced by dexamethasone. Dexamethasone did not affect the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA or 18S RNA content of adipocytes. Insulin increased leptin release by adipocytes in both the absence and presence of dexamethasone. Although insulin also prevented the loss of leptin mRNA, this effect was less than that observed for GAPDH mRNA or 18S RNA content. In isolated adipocytes, the loss of almost half the 18S RNA content over a 24-hour incubation was prevented in the presence of insulin but not oxytocin or epidermal growth factor (EGF). The specific beta3 catecholamine agonist CI 316,243 inhibited the effects of dexamethasone on leptin release and leptin mRNA accumulation, as did EGF, without affecting 18S RNA content. Oxytocin inhibited the increase in leptin release due to dexamethasone without affecting leptin mRNA levels. These data indicate that although dexamethasone and insulin are positive regulators of leptin release, only dexamethasone specifically prevented the loss of leptin mRNA in cultured rat adipocytes. In contrast, insulin, but not dexamethasone, prevented the marked loss in 18S RNA observed over a 24-hour incubation of rat adipocytes.
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PMID:Hormonal regulation of 18S RNA, leptin mRNA, and leptin release in adipocytes from hypothyroid rats. 986 73

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