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)

Specificity of binding of 3H-labeled arginine vasopressin [( 3H]AVP), down-regulation of receptors, and desensitization were studied in anterior pituitary glands of both Wistar and Brattleboro rats. Studies using both crude membrane fractions and isolated cells of anterior pituitaries revealed the presence of a single population of binding sites with a Kd of approximately 1 nM. The receptor recognized the following peptides, with AVP = lysine vasopressin = vasotocin greater than oxytocin = 1-deamino-(8-D-AVP) greater than d-(CH2)5-Tyr-(Me)-Val4-AVP greater than 1-deaminopenicillamine-(Val4-D-Arg8)VP. Neither corticotropin-releasing factor (CRF) nor any of the neuropeptides tested, including AVP ring and tail fragments, competed for tracer binding. Increased extracellular vasopressin levels due to chronic injections or long term adrenalectomy decreased receptor density by 80%, while oxytocin was less effective than AVP. Comparing binding data in Brattleboro homozygotes and heterozygotes revealed that AVP levels within the physiological range could down-regulate pituitary receptors as well. This could not be caused by occupation of sites by endogeneous vasopressin, since injection of large doses of peptide decreased tracer binding by less than 10%. Loss of pituitary receptors reduced 1) enhancement by AVP of CRF-induced cAMP accumulation, 2) intrinsic CRF-like activity and 3) synergistic effect of AVP on ACTH secretion elicited by CRF. This study thus provides evidence for the presence of highly specific vasopressin receptors in the anterior pituitary, which may undergo homologous down-regulation and desensitization in terms of cAMP production and ACTH release.
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PMID:Specific receptors for vasopressin in the pituitary gland: evidence for down-regulation and desensitization to adrenocorticotropin-releasing factors. 298 73

To investigate the mechanism by which ACTH secretion is inhibited during hypothermia, hypophysial portal blood was collected from euthermic and hypothermic rats, and the concentrations of corticotropin-releasing factor (CRF), vasopressin (AVP), and oxytocin (OT) were measured by RIA. Whereas CRF levels in portal plasma were not different in the two groups, AVP and OT levels were significantly lower in hypothermic rats. The concentration of AVP and OT in peripheral plasma was also significantly lower in hypothermic rats compared with euthermic controls. The pituitary responsiveness to CRF during hypothermia was tested in vivo and in vitro. In pentobarbital-anesthetized male rats injected iv with 0.1 or 1.0 nmol CRF, the ACTH response was significantly smaller in hypothermic compared with euthermic animals. However, hemipituitaries superfused at 31 C released the same amount of ACTH in response to 1 nM CRF as hemipituitaries superfused at 37 C (31 C, 541 +/- 90 pg; 37 C, 563 +/- 29 pg) despite reduced baseline secretion (31 C, 77 +/- 10 pg/10 min; 37 C, 114 +/- 14 pg/10 min; P less than 0.05). The data suggest that the inhibition of ACTH secretion during hypothermia is mediated by decreased hypothalamic secretion of AVP and OT which in turn decreases the pituitary responsiveness to CRF.
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PMID:Inhibition of corticotropin release during hypothermia: the role of corticotropin-releasing factor, vasopressin, and oxytocin. 298 77

Experiments were designed to study the effects of oxytocin on canine basilar and femoral arteries and to compare these with the effects of vasopressin. Rings of the arteries were suspended in physiological salt solution for isometric tension recording. Oxytocin and vasopressin caused endothelium-dependent relaxation of basilar arteries contracted with prostaglandin F2 alpha. Vasopressin was more potent than oxytocin. In the femoral artery, the two hormones caused endothelium-independent contractions with the same order of potency. The relaxations of the basilar artery occurred at lower concentrations of each substance than the contractions of the femoral artery. The relaxations in response to both agonists were inhibited competitively, and the contractions noncompetitively, by the V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP; the antagonist did not affect endothelium-dependent relaxations in response to bradykinin. Thus, both oxytocin and vasopressin cause endothelium-dependent relaxation of the basilar artery by activating V1-vasopressinergic receptors; the contractions of femoral arteries that they cause also may be mediated in part by V1-vasopressinergic receptors.
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PMID:Oxytocin causes endothelium-dependent relaxations of canine basilar arteries by activating V1-vasopressinergic receptors. 300 Dec 82

Effects of vasopressin (AVP), oxytocin (OXY), norepinephrine (NE), and glucose on the single-unit activity of hypothalamic ventromedial nucleus (VMN) in tissue slices were studied. While AVP was exclusively excitatory on 58% of the neurons, OXY could be excitatory or inhibitory and affected only 42% of the neurons. There was no correlation between the responses to these two peptides. Each of these two peptides could desensitize neuronal response to itself, but did not cross-desensitize responses to each other. These results indicate that AVP and OXY do not act on the same population of VMN neurons through the same cellular mechanism. Furthermore, only the responses to AVP were correlated to responses to glucose and NE, two agents relevant to central regulation of feeding. This correlation with responses to feeding-relevant agents and the exclusively excitatory action on the VMN, which is involved in the regulation of feeding, suggest that AVP can play a role in the regulation of feeding, particularly the feeding induced by the injection of NE into the paraventricular nucleus, that is known to alter AVP release.
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PMID:Vasopressin excites ventromedial hypothalamic glucose-responsive neurons in vitro. 301 71

The regulation of pituitary vasopressin (VP) receptor concentration was investigated in rats with antero-lateral cuts (ALC) placed around the hypothalamus, as well as in Brattleboro homozygotes (HO) that genetically suffer from a lack of AVP. Hypothalamic ALCs caused a reduction in (3H)-AVP binding, while counteracting the dramatic fall in binding that normally occurs after adrenalectomy. Surprisingly, in HO rats, long-term adrenalectomy did cause pituitary AVP receptor number to decrease to an extent similar to that seen in normal rats. However, the receptor disappeared twice as rapidly in heterozygote controls than in HO animals, with calculated half-lives of 1.1 and 2.0 days, respectively. In HO, chronic administration of VP reduced receptor concentration by about 80%, while the same dose of oxytocin (OT) produced only a 20-30% reduction. Whereas dexamethasone injections did reverse the depressing effect of adrenalectomy on pituitary AVP receptors, they failed to enhance binding in sham-operated controls, treated or not with VP; thereby suggesting a central site of action of the steroid. In contrast, in rats with hypothalamic ALCs (i.e. with the pituitary lacking central control), corticosterone implants did antagonize the reduction in receptor density caused by adrenalectomy. We conclude that the pituitary AVP receptor system lies mainly under control of the central nervous system, through a mechanism of action that not only seems to imply AVP and OT, but probably also some other hypothalamic factor(s). Glucocorticoids appear to exert a dual effect, acting indirectly through negative feedback control of neuropeptide release and, possibly, also directly on the pituitary to regulate binding sites.
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PMID:Central nervous system control of pituitary vasopressin receptors: evidence for involvement of multiple factors. 301 13

In this study, we examined whether the mechanisms mediating the induction of grooming behavior by oxytocin (OT) is similar to mechanisms mediating the effects of OT on uterine contractility. Sprague-Dawley strain female rats were injected intracerebroventricularly (ICV) with OT or OT analogues and then were observed for grooming behaviors 25 minutes later for 30 minutes. The uterotonic analogue deamino-OT injected ICV at equimolar doses to 1 microgram OT significantly elevated grooming scores although less than did OT. Other agonist analogues were not effective in inducing an increase in grooming behavior. The simultaneous ICV injection of the analogue [Pen1, Phe2, Thr4, delta 3, 4Pro7, Orn8]-OT, which blocked the effects of OT on uterine contractility, also blocked the effect of OT on grooming behavior. Injection of the same dose of this antagonist analogue did not effect the increased grooming behavior after AVP injection. Pretreatment with 5 mg/kg of the prostaglandin synthetase inhibitor indomethacin significantly inhibited OT-induced grooming. We have concluded from these data that the mechanism underlying the effect of OT on grooming is similar to its effects on uterine contractility in some respects. However, observations that the OT antagonist analogue blocked OT- but not AVP-induced grooming may suggest that more than one receptor or mechanism exists by which nonapeptides initiate excessive grooming.
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PMID:Is oxytocin-induced grooming mediated by uterine-like receptors? 302 Apr 70

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

Changes in immunostaining, median eminence content, and secretion into the hypophysial-portal circulation of immunoreactive CRF (irCRF), arginine vasopressin (irAVP), and oxytocin (irOT) were directly evaluated after pharmacological adrenalectomy (PHADX). Mean circulating levels of ACTH rose from 270 +/- 57 (+/- SE) to 1560 +/- 283 pg/ml after 72 h of treatment with metyrapone and aminoglutethimide. Initially, hypophysial-portal plasma irCRF levels decreased to 52.6% (12 h) and 21.7% (24 h) of control levels (230 +/- 41 pg/ml). Accompanying changes in the patterns of CRF immunostaining in the paraventricular nuclei (PVN) or in median eminence irCRF content at 24 h did not parallel alterations in portal plasma irCRF levels at this time. By 72 h posttreatment, portal irCRF levels were elevated 2.2-fold, while the number of detectable CRF-positive perikarya in the PVN increased 3.0-fold. The mean hypophysial-portal plasma irAVP concentration was unchanged from the control value (1312 +/- 287 pg/ml) at 12 h, but was only 34.9% of the control value at 24 h. Inverse changes in median eminence irAVP content were noted at these times, whereas the number of AVP-immunostained cells exhibited a tendency toward an increase at 24 h, in parallel with significantly increased content. By 72 h post-PHADX, portal irAVP, median eminence irAVP content, irAVP immunostaining intensity, and AVP-immunopositive cell number were elevated. Approximately 64% of CRF-positive perikarya in the parvocellular PVN costained for AVP at this time, whereas no colocalization was evident in untreated rats. These changes were prevented by corticosterone replacement. irOT staining intensity, irOT-positive cell number, median eminence irOT content, and portal plasma irOT concentration remained stable at all times examined. We conclude that: removal of adrenal steroids by PHADX results in a sequence of changes in CRF and AVP within the PVN (as determined by immunocytochemistry) and the median eminence (as determined by peptide content) similar to those observed after surgical adrenalectomy; after steroid removal the secretion of both irCRF and irAVP changes in a biphasic manner characterized by reduced secretion at 24 h and greatly enhanced secretion at 72 h; neither immunostaining nor median eminence content alone proved to be a reliable index or secretory activity during the initial phases of steroid blockade; and the hypophysiotropic OT system of normal male rats appears to be insensitive to adrenal steroid influences.
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PMID:Hypophysial-portal plasma levels, median eminence content, and immunohistochemical staining of corticotropin-releasing factor, arginine vasopressin, and oxytocin after pharmacological adrenalectomy. 303 Jun 97

Administration of lithium chloride and copper sulfate to adult monkeys caused marked elevations in plasma vasopressin (AVP) levels without significant increases in plasma oxytocin (OT) levels. Emesis was produced in five of the seven animals given these agents, in support of nausea as the main stimulus to AVP release. A similar pattern of AVP release without OT release was found after administration of cholecystokinin (CCK). Although most monkeys vomited in response to 10 micrograms/kg of CCK, a significant increase in plasma AVP levels also was produced with a dose of 1 microgram/kg, which did not produce emesis in any animal. These findings are in marked contrast with previous results in rats, which indicated that lithium chloride, copper sulfate, and CCK each stimulated OT rather than AVP release. Despite this interspecies difference, the significant neurohypophysial hormone secretion in response to both nausea-producing agents and CCK suggests that AVP secretion in monkeys, similar to OT secretion in rats, might reflect activation of central pathways mediating nausea and/or inhibition of food intake, even when overt illness is not produced.
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PMID:Vasopressin release in response to nausea-producing agents and cholecystokinin in monkeys. 303 8

Our laboratory has reported previously the characteristics of specific AVP binding to rat hippocampal synaptic membranes (SPM) in the presence of Ni2+ [Costantini MG, Pearlmutter AF: J Biol Chem 259: 11739-11745, 1984]. We extended our investigation to determine the effects of Ni2+, (AVP), and AVP analogs on SPM protein phosphorylation. Ni2+ (5 mM) caused a dramatic reduction in phosphorylation of most SPM phosphoproteins. The most prominent protein which is phosphorylated in SPM has a molecular weight of 48 kilodaltons (KDa) and has been named B50 or F1; this protein shows altered phosphorylation in vitro in response to long-term potentiation in vivo as well as changes induced by exposure of SPM to ACTH (1-24), dopamine, and somatostatin. AVP and related peptides reduced phosphorylation of this pre-synaptic phosphoprotein in the following order of potency: AVP = oxytocin greater than DG-AVP greater than dDAVP greater than d(CH2)5Tyr(Me)AVP = [pGlu4,Cyt6]AVP-(4-9). Except for the pressor antagonist d(CH2)5Tyr(Me)AVP, this corresponds to their relative efficacy in displacing 3H-AVP from high-affinity specific binding sites on rat hippocampal synaptic membranes. Ni2+ did not alter the degree of inhibition caused by the peptides. When SPM were treated with AVP after the attainment of maximum 32P incorporation, AVP inhibited dephosphorylation over a 30-min period. Our results show that AVP can alter both phosphorylation and dephosphorylation of hippocampal SPM phosphoproteins in vitro; the direction of these effects depends upon experimental conditions. Since B50/F1 is known to be a substrate for protein kinase C, AVP may act by inhibition of protein kinase C activity, either directly or indirectly.
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PMID:Effects of arginine vasopressin on protein phosphorylation in rat hippocampal synaptic membranes. 303 58


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