Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenomas of the pars intermedia from 19 horses and normal pituitary glands from seven horses were evaluated histologically and immunocytochemically for adrenocorticotropic hormone (ACTH), alpha-melanocyte-stimulating hormone (alpha-MSH), beta-endorphin (beta-END), proopiomelanocortin (POMC), prolactin, neuron specific enolase, and glial fibrillary acidic protein (GFAP). The 26 horses ranged in age from 7 to 31 years. Histologically, all adenomas had a uniform pattern characterized by cords of large columnar cells forming palisades and pseudoacini separated by a delicate fibrovascular stroma. Immunostaining of adenomas derived from the pars intermedia was similar to that of non-neoplastic equine pars intermedia. An immunocytochemical evaluation revealed a diffuse, strong cytoplasmic reaction for POMC, a moderate to strong reaction for alpha-MSH and beta-END, a weak reaction for ACTH, and negative immunostaining for prolactin, GFAP, and neuron specific enolase in the adenomas. The unique clinicopathologic syndrome that develops in horses with pituitary adenomas appears to be the result of an over-production of POMC-derived peptides in addition to space-occupying effects resulting in dysfunction of the hypothalamus and neurohypophysis.
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PMID:Immunocytochemical demonstration of proopiomelanocortin-derived peptides in pituitary adenomas of the pars intermedia in horses. 217 80

In the light of evidence for endogenous opioid peptide involvement in the modulation of pituitary hormone release and in the body's overall response to stress, the aim of the present study was to determine the beta-endorphin-like immunoreactivity (beta-END-LI) in the blood plasma of ewes during different phases of the estrous cycle and in anestrous ewes subjected to acute or intermittent prolonged footshocks. The highest concentration of beta-END-LI was found in the blood plasma during the luteal phase and lowest one during the follicular stage at proestrus. Nearly equal concentrations of beta-END-LI were determined at estrus and metestrus; their values were over 10 times lower than those observed in the luteal phase. Acute stress caused transient increase of beta-END-LI in the blood plasma of anestrous ewes, with a peak after 15-30 min of footshock application and changes in the molar ratio of beta-LPH to beta-endorphin. No apparent increase in mean daily levels of beta-END-LI was noted in ewes subjected to prolonged footshocking; however, on the day after stimulation beta-END-LI concentration decreased below control values. These results indicate that: 1. secretion of beta-END-LI varies during different phases of the estrous cycle, 2. acute stress is a potent activator for beta-END-LI secretion, 3. no apparent increase of beta-END-LI in the blood plasma of ewes subjected to prolonged stress concomitant with accumulation of this material in pituitary (Polkowska and Przekop, 1988) supports the idea, that prolonged stress augments the synthesis of beta-END-LI but not its release.
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PMID:Changes in beta-endorphin-like-immunoreactivity in the blood plasma of ewes during estrous cycle and in anestrous ewes under stress condition. 224 20

The effect of the endogenous opioid peptides, methionine-enkephalin (Met-ENK), beta-endorphin (beta-END) and dynorphin-(1-17) (DYN) on the aversive behavior produced by intrathecal (i.t.) administration of substance P (SP) was studied in mice. A low dose of i.t. administered Met-ENK gave a marked reduction of the SP-induced response. In the tail-flick assay, such doses of Met-ENK were ineffective in producing antinociception. At much higher doses, however, Met-ENK obtained antinociceptive activity. In contrast, beta-END and DYN had about the same potency in inhibiting the SP-induced behavioural response and in the tail-flick test, respectively. These results suggest that opioid peptides, particularly enkephalin neurons in the spinal cord influence SP-induced aversive behaviour.
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PMID:Enkephalins interact with substance P-induced aversive behaviour in mice. 245 88

Interleukin-1 (IL-1) exerts a wide variety of biological effects on various cell types and may be regarded as a pleiotropic peptide hormone. Biological evidence suggests that IL-1 participates in the modulation of central nervous system physiology and behaviour in a fashion characteristic of neuroendocrine hormones. In this investigation, recombinant (r) human (h) IL-1 and r mouse (m) IL-1 were examined for their modulation of opioid peptide receptor binding in vitro. Experiments were performed on frozen sections of rat brain. Receptor binding of radiolabeled substance P and of radiolabeled neurotensin were not significantly affected by the presence of rIL-1s. Recombinant IL-1s, however, significantly enhanced specific binding of 125I-beta-endorphin (125I-beta-END) and of D-ala2-(tyrosyl-3,5-3H)enkephalin-(5-D-leucine) (3H-D-ALA), equipotently and in a concentration-dependent manner with maximal activity occurring at a concentration of 10 LAF units/ml. The increased binding of 125I-beta-END and 3H-D-ALA was blocked steroselectively by (-)-naloxone and by etorphine, suggesting detection of opiate receptors. In addition, brain distribution patterns of receptors labeled in the presence of rIL-1s corresponded to patterns previously published for opiate receptors. Autoradiographic visualization of receptors revealed that rIL-1s in the different areas of the brain exert their effect on opioid binding with comparable potencies. The data suggest that certain central nervous system effects of IL-1s may be mediated by their selective interaction with opiatergic systems at the receptor level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interleukin-1 interaction with neuroregulatory systems: selective enhancement by recombinant human and mouse interleukin-1 of in vitro opioid peptide receptor binding in rat brain. 246 86

1. The effects of intravenous (i.v.) morphine on adrenocorticotrophic hormone (ACTH), beta-endorphin (beta-END), total catecholamines (CA) and histamine (HIS) plasma concentrations, were determined in anaesthetized dogs at 30 degrees C and 37 degrees C. 2. Hypothermia initially increased CA levels by 29%, but the values returned to baseline after 2 h. Morphine (1 mg/kg, i.v.) produced a significant decrease in CA both at 37 degrees C and 30 degrees C (34% and 54%, respectively). Subsequent administration of naloxone (1 mg/kg, i.v.) significantly increased CA levels in both groups. 3. Hypothermia per se had no effect on ACTH, beta-END, and HIS concentrations. Morphine produced a significant increase in pituitary hormones and HIS, in hypothermic but not in normothermic animals. Morphine concentrations were significantly higher at 30 degrees C during the first 45 min. 4. The results suggest that the effects of morphine on hormonal and histamine release observed at 30 degrees C are concentration-dependent and related to changes in morphine pharmacokinetics.
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PMID:Hypothermia enhances the effects of morphine on hormonal and histamine release. 247 84

A quantitative assessment of the carotid sinus baroreflex release of endogenous plasma beta-endorphin-like immunoreactive material has been established. The carotid sinuses of 12 pentobarbital sodium-anesthetized dogs were isolated bilaterally and perfused with a constant pressure maintained by infusion or withdrawal of normal saline. Mean arterial pressure (MAP) and heart rate (HR) were monitored. Carotid sinus pressure (CSP) was changed from 200 to 50 mmHg in 25 mmHg steps before and after vagotomy. At each interval of CSP, 10 ml mixed venous blood were collected, and beta-endorphin-like peptides were extracted from plasma and assayed. Concentrations of plasma beta-endorphin-like material were determined by radioimmunoassay. Sigmoidal responses of MAP and HR were revealed during changes in CSP. No significant differences in beta-endorphin-like immunoreactivity (beta-END-L-I) were measured at CSP of 200 and 50 in the intact condition (35.9 +/- 3.9 and 35.0 +/- 6.4 fm/ml, respectively). However, after vagotomy, beta-END-L-I measured at 50 mmHg CSP was significantly elevated to 53.3 +/- 5.2 fm/ml compared with the value of 35.5 +/- 7.2 fm/ml at CSP of 200 mmHg. The results suggest that the release of beta-endorphin is modulated by the action of the carotid baroreflex as a normal component of an integrated efferent response. However, this response is normally buffered by reflexes with vagal afferents.
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PMID:Carotid sinus baroreflex control of beta-endorphin release in anesthetized dogs. 252 79

Pro-opiomelanocortin (POMC) is the precursor to several pituitary hormones including adrenocorticotropic hormone and beta-endorphin (beta-END). POMC is also expressed in the brain, predominantly in discrete neuronal cell populations of the hypothalamus. In the pituitary and brain, POMC undergoes tissue-specific proteolysis to release different bioactive peptides. POMC processing in neuronal cell lines was studied after infection of PC12 and Neuro2A cells with a recombinant retrovirus carrying the porcine POMC cDNA. Our results indicate that both cell lines synthesize and target POMC to the regulated secretory pathway. Only the Neuro2A cells, however, can achieve proteolytic processing of POMC. Chromatographic and immunological characterization of the POMC-related material showed that beta-lipotropin (beta-LPH) and nonacetylated beta-END(1-31) are major maturation products of POMC in these cells. Release of both beta-LPH and beta-END(1-31) from infected Neuro2A cells can be stimulated by secretagogues in a calcium-dependent manner. Taken together, our results suggest that the cellular machinery of Neuro2A cells can recognize a foreign prohormone, target it to neurosecretory vesicles, process it into biologically active peptides, and secrete it in a manner characteristic to peptidergic neurons.
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PMID:Targeting and processing of pro-opiomelanocortin in neuronal cell lines. 252 37

In response to stressors involving tissue injury, pituitary corticotroph secretion of immunoreactive beta-endorphin (iB-END) could be either due to release of hypothalamic factors such as corticotropin-releasing factor (CRF) or to release of a tissue factor from the periphery. In the present experiments, we investigated whether inflamed tissue releases a factor which evokes pituitary secretion of iB-END. In an initial experiment, rats with an inflamed hindpaw due to carrageenan injection had significantly greater levels of circulating iB-END as compared to rats with saline-injected paws. Removal of afferent input, by hindlimb denervation, failed to block the carrageenan-induced increase in iB-END levels. Subcutaneous perfusates were then collected from inflamed and control hindlimbs and applied to rat anterior pituitary cell cultures. Pituitary release of iB-END due to administration of perfusate from inflamed paws was significantly greater than iB-END release due to perfusate from saline-injected paws or to basal release. The releasing activity in the perfusates was blocked in calcium-free medium and was not due to a direct action of carrageenan, bradykinin, substance P or calcitonin gene-related peptide. The results indicate that inflamed tissue releases a CRF-like factor which stimulates iB-END release both in the denervated rat and cultured pituitary cells.
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PMID:Release from inflamed tissue of a substance with properties similar to corticotropin-releasing factor. 252 75

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

The present study evaluated the hypothesis that increased plasma levels of epinephrine (EPI) stimulate immunoreactive beta-endorphin (i beta END) secretion in humans experiencing a mild stress. The stressor consisted of intraoral injections of a local anesthetic solution (with or without EPI) just before the surgical extraction of impacted third molars in 26 awake unsedated patients. The EPI group experienced a 30-fold increase in plasma EPI levels by 2 min after injection; these concentrations were physiologically active, as evidenced by increased pulse rate and systolic blood pressure. However, compared to a no EPI control group the EPI group had a significantly reduced i beta END response to the stressor, as evaluated by comparison of plasma levels at individual time points, maximal increases in plasma i beta END levels, and areas under the time-response curve. Whereas there was no association between plasma levels of EPI and i beta END in the EPI group (r = 0.119; P = NS), EPI and i beta END levels were strongly related in the no EPI group (r = 0.82; P less than 0.001). These results do not support the hypothesis of a stimulatory effect for EPI on i beta END release and, instead, suggest that an inhibitory relationship may exist in humans experiencing stress. The association between EPI and i beta END responses observed in the control group during this form of stress appears to be due to activation of a common central neural element.
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PMID:Epinephrine suppresses stress-induced increases in plasma immunoreactive beta-endorphin in humans. 252 44


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