UNIPROT:P01189 - FACTA Search

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Query: UNIPROT:P01189 (beta-endorphin)
21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study examines whether a correlation exists between cyclic nucleotides and the mechanism of action of arginine vasopressin (AVP) on adrenocorticotropin hormone (ACTH) secretion from pituitary corticotrophs. Incubation of cultured anterior pituitary cells with 3-isobutyl-1-methylxanthine (IBMX) or Rolipram elevated the basal intracellular content of both adenosine 3':5'-cyclic monophosphate (cAMP) and guanosine 3':5'-cyclic monophosphate (cGMP) or cAMP alone, respectively. Both IBMX and Rolipram enhanced the AVP-stimulated secretion of ACTH in cultured anterior pituitary cells, but not in AtT-20 corticotrophs which lack functional AVP receptors. Rolipram was less potent than IBMX in this regard, which suggests a possible involvement of cGMP. In contrast, both drugs showed similar potency to stimulate CRF-induced ACTH secretion. Incubation of pituitary cells with atrial natriuretic factor elevated tissue cGMP levels and increased the ACTH response to AVP. The results of this study show that, although AVP fails to directly affect the levels of cAMP and cGMP in anterior pituitary cells, the stimulatory effect of AVP on ACTH secretion was modulated by the cellular cAMP content.
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PMID:Indirect relationship between vasopressin-induced secretion of ACTH and cyclic nucleotides in cultured anterior pituitary cells. 246 10

Single and dual immunohistochemical staining techniques were used to assay the effects of disruption of brain stem catecholaminergic inputs on corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) immunoreactivity in parvocellular neurosecretory neurons of the paraventricular nucleus of the hypothalamus (PVH) in normal and in adrenalectomized (ADX) rats treated with dexamethasone or vehicle. The results may be summarized as follows: (1) In adrenally intact rats, confirmed unilateral transection of ascending catecholaminergic pathways near their origins in the medulla produced a decrement in the number of CRF-immunoreactive cells that could be detected on the side of the brain ipsilateral to the cut. No effect on AVP immunoreactivity in the parvocellular division of the PVH was evident. Staining for both peptides in terminals in the external lamina of the median eminence tended to show modest decreases on the lesioned side of the brain. Compatible results were obtained in comparing the effects of bilateral transections with controls. (2) Unilaterally lesioned ADX rats treated with vehicle showed the expected enhancement in CRF immunostaining in the parvocellular division of the PVH, though the response on the side ipsilateral to the lesion was blunted relative to that seen contralaterally; the effect of ADX on AVP immunoreactivity on the ipsilateral side was more markedly reduced, but still showed evidence of enhancement (i.e., could be colocalized in some CRF immunoreactive perikarya). (3) Unilaterally lesioned ADX rats treated with dexamethasone showed no evidence of enhanced CRF or AVP immunoreactivity in perikarya or terminals on either side of the brain. The generally lower levels of staining for both peptides seen on the lesioned side across conditions suggest that the effect of interruption of ascending catecholaminergic pathways on peptide dynamics in the PVH is dissimilar to that of ADX, is manifested via different mechanisms, and that at least some types of feedback inhibition of corticotropin-releasing peptides by adrenal steroids do not require intact catecholaminergic inputs to be exhibited.
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PMID:Effects of catecholamine-depleting medullary knife cuts on corticotropin-releasing factor and vasopressin immunoreactivity in the hypothalamus of normal and steroid-manipulated rats. 246 27

Corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) stimulate the secretion of beta-endorphin by human PBMC. It is shown here that peripheral blood B cells are responsible for the production of beta-endorphin after culture with CRF and AVP. The presence of CD14+ monocytes is, however, a prerequisite for the enhancing activity of CRF and AVP. The data presented here show that rIL-1 beta can replace CRF and AVP, whereas a mAb directed against IL-1 abrogates the response to CRF and AVP. These results indicate that IL-1 mediates the effect of CRF and AVP on beta-endorphin production by human PBMC.
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PMID:The role of IL-1 in the corticotropin-releasing factor and arginine- vasopressin-induced secretion of immunoreactive beta-endorphin by human peripheral blood mononuclear cells. 252 82

To assess central nervous system cholinergic neuroendocrine regulation in Alzheimer's disease (AD), we measured plasma arginine vasopressin, beta-endorphin, and epinephrine responses to a cholinergic challenge elicited by intravenous administration of the acetylcholinesterase inhibitor physostigmine (0.0125 mg/kg) in male patients with AD (n = 12) and compared their responses with those of age-matched normal control subjects (n = 12). Physostigmine promptly increased plasma arginine vasopressin (tenfold), beta-endorphin (twofold to threefold) and epinephrine (threefold) levels in elderly control subjects. In contrast, patients with AD showed attenuated responses to physostigmine. When controls and patients with AD who experienced nausea (n = 2 and n = 6, respectively) were excluded, the arginine vasopressin, beta-endorphin, and epinephrine responses of patients with AD were significantly less than those of control subjects. These data suggest that the central nervous system cholinergic deterioration of AD results in decreased responsiveness of neuroendocrine systems that are regulated by central cholinergic mechanisms.
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PMID:Neuroendocrine responses to physostigmine in Alzheimer's disease. 252 15

The posterior pituitary contains a PRL-releasing factor (PRF), a small (less than 5000 mol wt) peptide which is distinct from known PRL secretagogues. The objectives of this study were to determine if posterior pituitary extracts specifically stimulate PRL release in vivo and to assess the relative contributions of oxytocin (OT), arginine vasopressin (AVP), and beta-endorphin (beta END) to the PRF activity of the extract. Rat posterior pituitaries or cerebellar tissue were extracted with 1.0 N acetic acid, boiled, and ultrafiltered through 5000 mol wt cutoff membranes. The eluates were treated with performic acid (which oxidizes disulfide bonds and methionine residues), lyophilized, and reconstituted in saline. Jugular blood was collected from conscious ovariectomized rats before and after intracarotid injection of test substances and was analyzed for PRL, LH, and GH by RIA. Injection of 0.3, 1.0, and 3.0, posterior pituitary equivalents increased plasma PRL levels by 2-, 8-, and 22-fold, respectively. PRL levels peaked within 5 min after the injection and returned to basal levels by 30 min. Plasma LH levels decreased slightly, and GH was unchanged. Cerebellar extracts did not affect plasma hormone levels. Injection of OT induced a 4-fold rise in plasma PRL levels. Oxidation of OT was well as AVP with performic acid abolished any PRL-releasing activity. Injection of beta END increased plasma PRL levels by 7-fold. Treatment of beta END with performic acid caused a 60% loss in its ability to release PRL. Pretreatment of rats with naloxone abolished the PRL-releasing effect of beta END, but did not alter the PRF activity of posterior pituitary extracts. We conclude that posterior pituitary extracts stimulate PRL release in vivo in the presence of an intact dopaminergic inhibition. This stimulation is rapid, dose dependent, and hormone specific. OT, AVP, and beta END do not contribute significantly to the PRF activity in the posterior pituitary extract.
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PMID:The posterior pituitary contains a potent prolactin-releasing factor: in vivo studies. 252 28

It is well established that in the pituitary gland corticotropin-releasing hormone (CRH) stimulates the release of beta-endorphin (beta-E) via a cAMP-linked mechanism. Studies of the mechanisms underlying the CRH stimulation of beta-E release from rat hypothalamic slices perifused in vitro are reported in this paper. The data indicate that both a cAMP-dependent and non-cAMP-dependent mechanism mediate the action of CRH in the hypothalamus. The presence of a cAMP-linked mechanism was suggested by the finding that cholera toxin (0.1-10 nM) and forskolin (2.5 x 10(-6) M), both of which act to raise intracellular cAMP levels, stimulated the release of beta-E. In both cases, no further stimulation was seen upon addition of CRH (10(-8)M). However, it was also found that preincubation of the tissue with pertussis toxin (PTX; 100 ng/ml) prevented both the CRH- and forskolin-stimulated release of beta-E. This indicated that, in addition to the cAMP-linked mechanism, a further messenger system which is connected to a PTX-sensitive G-protein may also play a role. The latter observation also implied that a further substance, which utilizes a separate second messenger system, might be involved in the CRH stimulation of beta-E release. In this regard the role of arginine vasopressin (AVP) was investigated due to the known interaction between CRH and AVP in the pituitary gland. AVP (10(-12) to 10(-6)M) itself potently and dose-dependently stimulated beta-E release, producing a maximal increase of 220% above basal levels. The AVP-induced release of beta-E was abolished in PTX-pretreated hypothalami. The apparently obligatory requirement of AVP for the CRH-stimulation of beta-E release was illustrated by the finding that blockade of AVP receptors using the AVP antagonist d(CH2)5 [Tyr(OEt)2,Val4]-AVP almost completely attenuated the CRH-stimulated release of beta-E. Furthermore, in the presence of a high concentration of AVP (10(-6)M) no further stimulation of release was seen with CRH (10(-8)M). These data therefore strongly indicate that CRH acts via the intermediacy of AVP to release beta-E from hypothalamic slices in vitro and that two separate second messenger systems are involved: a cAMP-linked mechanism connected to a cholera toxin-sensitive G-protein (CRH) and a second system linked to a PTX-sensitive G-protein (AVP).
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PMID:A two-step mechanism by which corticotropin-releasing hormone releases hypothalamic beta-endorphin: the role of vasopressin and G-proteins. 252 50

The evidence for an analgesic effect arising from increased peripheral concentrations of beta-endorphin (beta-EP) in various animal species is controversial, and has not been fully evaluated in the sheep. To stimulate beta-EP release, ovine corticotropin-releasing factor (oCRF) and arginine vasopressin (AVP) were injected intravenously (iv) into a group of 12 out of 24 sheep, 15 min prior to minor surgery on all sheep. This brought about significant increases (P less than 0.01) in plasma beta-endorphin (beta-EP) and cortisol concentrations, relative to the non-injected control sheep, 15-30 min after injection. Ultrafiltration indicated that less than 30% of the released beta-EP immunoreactivity was present as higher molecular weight forms (mol. wt greater than 10,000) and that the majority (about 75%) of the beta-EP was probably bound to plasma proteins. By 75 min after injection there was no significant difference in plasma beta-EP or cortisol concentrations between the two groups of sheep. Consistent with previous observations the sheep showed a characteristic aversive behavior to the human handler following surgery, lasting several days. This behavior appeared to be unaffected by a pre-operative increase in peripheral plasma beta-EP, and may indicate that this increase in beta-EP was not sufficiently analgesic to block the cognitive response to the operation, or long-lasting enough to prevent the perception of post-operative soreness.
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PMID:Effects of ovine corticotropin-releasing factor and vasopressin on plasma beta-endorphin, cortisol and behavior after minor surgery in sheep. 252 27

Neuroendocrine responses to the hypothalamic pituitary-adrenal axis following electroconvulsive treatment (ECT) were evaluated in twelve depressed (6 males/6 females) patients. Plasma concentrations of arginine vasopressin (AVP), corticotropin releasing factor (CRF), corticotropin (ACTH), and cortisol were measured using radioimmunological methods at four different ECT occasions. At each occasion plasma samples were taken immediately before ECT, at the recovery of spontaneous breathing and at 10 and 30 minutes after the ECT. No changes were observed in the plasma CRF concentrations. A large and rapid increase in plasma AVP concentrations was seen after the ECTs. This was followed by increased plasma ACTH and plasma cortisol levels. It is generally believed that AVP exerts a modulatory potentiating action on the CRF-induced ACTH release. The present results demonstrate that AVP per se can cause a release of ACTH from the anterior pituitary.
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PMID:Arginine vasopressin, but not corticotropin releasing factor, is a potent stimulator of adrenocorticotropic hormone following electroconvulsive treatment. 253 73

The proportions of different molecular weight forms of adrenocorticotropic hormone (ACTH) present in pituitary extracts, cultured pituitary cell extracts and cell-derived incubation media from fetal and postnatal sheep have been determined. When pituitary extracts, cell extracts, and incubation media were subjected to gel filtration on Sephadex G50 fine, three forms of ACTH were always observed. 'Big' ACTH eluted in the void volume of the column; 'intermediate' ACTH eluted between 'big' ACTH and human ACTH, and 'little' ACTH eluted in the same fractions as human ACTH. High amounts of 'big' and 'intermediate' ACTH were observed in extracts of cultured pituitary cells from both fetuses and newborn lambs, whereas very few 'little' ACTH was found. Conversely, in incubation media, the predominant form of ACTH was always 'little' ACTH. The relative proportion of these three forms of ACTH were rather similar in pituitary extracts and in cell-derived incubation media from newborn lambs. However, for fetuses the proportions of 'big' and 'intermediate' ACTH were higher, whereas that of 'little' ACTH was lower in pituitary extracts than in cell-derived incubation media. Neither corticotropin-releasing factor (oCRF) nor arginine vasopressin (AVP), separately or in combination, was able to modify the relative proportion of the three forms of ACTH released by pituitary cells from newborns. Conversely, for fetal cells, the proportion of 'little' ACTH released in the medium was higher in the presence of oCRF and/or AVP than under control conditions. The proportion of 'little' ACTH released by pituitary cells in the absence of stimulating factor increased linearly between 63 days of gestation and 150 days postpartum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adrenocorticotropic hormone released by pituitary cells from ovine fetuses and lambs. Polymorphism and biological activity. 254 58

Studies were undertaken to characterize the secretion of corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) into the hypophysial-portal circulation of the conscious sheep. In addition, we examined the temporal relationship between the secretion of these two hypothalamic peptides and the secretion of three pro-opiomelanocortin peptides--adrenocorticotropic hormone (ACTH), ir-beta-endorphin, and ir-alpha-melanocyte-stimulating hormone--and cortisol and determined the effects of an audiovisual emotional stimulus and insulin-induced hypoglycemia on the entire hypothalamic-pituitary-adrenal axis. In the basal state, the secretion of CRF, AVP, the three pro-opiomelanocortin peptides, and cortisol was pulsatile in nature, and three CRF and AVP pulse patterns were observed: a concordant increase in CRF and AVP, an isolated rise in CRF, and an isolated increase in AVP. In 4 of the 5 animals, a 3-min audiovisual stress (barking dog) rapidly increased the plasma levels of all the measured substances, although the magnitude and duration of the effect differed markedly between the animals. Insulin-induced hypoglycemia markedly increased AVP and, to a lesser extent, CRF concentrations in portal plasma and thereby altered the CRF:AVP molar ratio. Although pituitary-adrenal activation was closely correlated with the increased hypothalamic activity, a strict 1:1 concordance between CRF/AVP secretion and ACTH secretion was not seen. The anesthetic ketamine selectively increased portal AVP concentrations to levels which exceeded those attained during hypoglycemia and rapidly activated the pituitary-adrenal axis. We conclude the following: (1) CRF and AVP are secreted by the hypothalamus in a pulsatile fashion; (2) ACTH secretion can be stimulated by increases in either CRF or AVP; (3) the absence of a strict 1:1 concordance between hypothalamic CRF/AVP release and pituitary ACTH secretion during stress may be partly due to the release of additional hypothalamic ACTH secretagogues; (4) the ability of both audiovisual stimuli and insulin-induced hypoglycemia to augment CRF and AVP secretion indicates that the paraventricular hypothalamus may be activated by a variety of neural inputs, and (5) the marked alteration of the CRF:AVP molar ratio during stress suggests that AVP may be an important ACTH secretagogue in vivo in the sheep.
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PMID:Studies of the secretion of corticotropin-releasing factor and arginine vasopressin into the hypophysial-portal circulation of the conscious sheep. I. Effect of an audiovisual stimulus and insulin-induced hypoglycemia. 254 60

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