Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The opioid peptide, beta-endorphin, originates from proopiomelanocortin (POMC) under the influence of corticotropin releasing hormone (CHR). It increases the threshold of pain and has a certain influence on the formation of hypophyseal hormones, especially in stress. It is found that beta-endorphin stimulates the secretion of prolactin, a growth hormone, and vasopressin; it inhibates formation of follicle-stimulating and luteinizating hormones, oxytocin and dopamine, and gonadotropin, a releasing hormone. The process of acetylization decreases its activity. The results of experimental trials revealed that acetylisation in the foetal period was absent. The aim of the study was to define beta-endorphin concentration during normal vaginal labor and Cesarean section. Samples of peripheral blood of patients with spontaneous vaginal labor (n = 15) and of those in whom labor was operatively terminated (Cesarean section) (n = 10), were analysed. Values of this opiate were determined in the umbilical cord of newborn infants, in the amniotic fluid and placental compartment. The obtained results were statistically analysed. In intrapartum beta-endorphins were significantly increased reaching the highest level during expulsion (326 pg/ml); in the placental compartment these values were higher (in retroplacental blood 514 pg/ml) reaching the highest value of 917 pg/ml, p less than 0.01 in the placenta. In Cesarean section beta-endorphin values in the peripheral blood showed no significant differences during spontaneous vaginal labor. However, increased values of this natural opiate were observed six hours after surgery. Beta-endorphin concentrations in the placental compartment and the placenta during normal vaginal labor were significantly higher in comparison with labor by Cesarean section (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The opioid peptide, beta-endorphin, in spontaneous vaginal delivery and cesarean section]. 180 97

Beta-endorphin is a peptide with morphine-like effects produced primarily in the anterior lobe of the pituitary gland. After its cleavage from the parent molecule, proopiomelanocortin, beta-endorphin is circulated via the blood stream to interact with specific opioid receptors located throughout the body. The peptide produces analgesia by inhibiting the firing of peripheral somatosensory fibers. It also affects other senses, such as vision, hearing, and smell. Whereas the ability to increase beta-endorphin secretion during times of surgical stress is positively correlated with amelioration of pain, the administration of exogenous opioids, such as fentanyl, reduces plasma beta-endorphin. Decreased beta-endorphin concentrations may play a role in trigeminal neuralgia, migraine headache, and rheumatoid arthritis.
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PMID:Peripheral beta-endorphin and pain modulation. 181 47

Seven women undergoing abdominal hysterectomy under halothane and nitrous oxide analgesia had plasma samples taken before, during and after surgery for assay of adrenocorticotrophin (ACTH), beta-endorphin, beta-lipotrophin and methionine (Met)-enkephalin immunoreactivity. Plasma ACTH, beta-endorphin and beta-lipotrophin all rose in parallel from the start of surgery and were unaffected by postoperative opiate analgesia. Plasma Met-enkephalin concentrations did not change significantly during the course of the surgery and immediate post-operative period, although the variance of the samples increased at the time of the first skin incision. These data indicate that the stress of surgery and post-operative pain, while producing marked elevations of proopiomelanocortin-derived peptides, are not associated with changes in plasma Met-enkephalin. These data exclude a role for circulating Met-enkephalin in the modulation of surgical pain but do not exclude such a role for beta-endorphin.
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PMID:The effect of surgery on plasma beta-endorphin and methionine-enkephalin. 285 64

Chronic arthritic pain was induced by intradermally inoculating rats at the tail-base with Mycobacterium butyricum, which results in swelling, inflammation, and hyperalgesia of the joints. These symptoms peak at 3 weeks after inoculation and disappear by 10 weeks. The following changes were seen at 3 weeks. Immunoreactive dynorphin (ir-Dyn) and ir-alpha-neo-endorphin (alpha-NE) manifested comparable patterns of change. Their levels were increased in the anterior, but not neurointermediate, pituitary. The thalamus showed a rise in ir-Dyn and ir-alpha-NE, but no alterations were seen in other brain regions. In each case, cervical, thoracic, and lumbosacral sections of the spinal cord showed a rise in ir-Dyn and ir-alpha-NE: This was most pronounced in the lumbosacral region, where the magnitude of these shifts correlated with the intensity of arthritic symptoms. In addition, a moderate elevation in ir-methionine-enkephalin (ME) was seen in lumbosacral spinal cord. In brain, ir was not changed. The level of ir-beta-endorphin (beta-EP) was elevated both in the plasma and the anterior, but not the neurointermediate, pituitary. In addition, the content of messenger RNA encoding the beta-EP precursor, proopiomelanocortin (POMC), was enhanced in the anterior lobe. Thus, there was a selective activation of synthesis of beta-EP in, and its secretion from, the anterior lobe. In no brain tissue did levels of ir-beta-EP change. At 10 weeks postinoculation, the above changes were no longer apparent, indicating their reversibility.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A model of chronic pain in the rat: response of multiple opioid systems to adjuvant-induced arthritis. 287 Nov 41

Acute stress promotes the secretion of prolactin (PRL) and of proopiomelanocortin (POMC)-derived peptides, adrenocorticotropic hormone and beta-endorphin, from the pituitary into the systemic circulation. The present study evaluates the influence of recurrent stress upon the biosynthetic activity of cells secreting these hormones in the rat. Chronic, intermittent, electrical foot-shock (3 mA,1 s duration, every 5 s for 30 min, twice daily) over a period of 1, 3 or 7 days caused an increase in messenger ribonucleic acid (mRNA) levels coding for POMC in the anterior pituitary. Maximally elevated mRNA levels were achieved after 3 days treatment (about 80% in excess of control values) which showed no further change at 7 days. These elevated levels of POMC mRNA were associated with increased levels of immunoreactive (ir)-beta-endorphin in the adenohypophysis following 7 days of stress treatment. In contrast, this treatment did not significantly alter mRNA levels coding for PRL in the anterior pituitary. Similarly, POMC mRNA levels in the intermediate/posterior pituitary were also not significantly altered during exposure to repeated stress. Similar changes in the biosynthesis of the pituitary hormones were seen in rats suffering from chronic arthritic pain for 3 weeks: there was an approximately 80% increase in POMC mRNA levels in the anterior pituitary which was associated with an increase in the levels of ir-beta-endorphin in this lobe and an increase in the plasma levels of ir-beta-endorphin. In contrast, there were no changes in the levels of mRNA coding for PRL in the adenohypophysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stress-induced alterations in the levels of messenger RNA coding for proopiomelanocortin and prolactin in rat pituitary. 294 92

The role of opioid peptides in modulating the nervous system adaptability has been demonstrated recently; proopiomelanocortin (POMC)-related peptides, in particular, serve in pain perception, in adaptation to stress, and in modulating higher brain functions. Primary headaches, besides pain, involve neuroendocrine/autonomic/adaptive processes as well as mood and personality factors. The view that primary headaches can be taken as a possible model of POMC-related peptides dysfunction led us to evaluate the resting plasma and CSF peptide levels and their plasma changes in response to various stimuli affecting their release. The data obtained from basal and dynamic studies agree with the concept that primary headaches are sustained by opioid system disturbance. In particular the reduced release of endogenous opioids by anterior pituitary in response to physical, endocrine or pharmacological stimuli agrees with a weak adaptive ability of headache sufferers. This impairment of endorphin responsiveness could play a key role in headache susceptibility to environmental stimuli. Primary headaches constitute a wide, intriguing field, including several subgroups bordering on "ischemic" and behavioral/affective disorders. The development of neuroendocrine techniques could be a useful means for supporting the clinical criteria identifying subpopulations of headache sufferers.
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PMID:Endorphin patterns within the headache spectrum disorders. 299 Jul 21

To determine whether opioid peptide-receptor pharmacological association found in vitro (e.g., enkephalin-delta, dynorphin-kappa) predict anatomical relationships in situ, immunocytochemical and receptor autoradiographic studies were carried out on adjacent sections from the same brains of formaldehyde-perfused rhesus monkeys. Apparent mu and kappa opioid receptors (labeled, respectively, by [3H] naloxone and [3H]bremazocine under different incubation conditions), but not delta opioid receptors (labeled by [3H]D-Ala2, D-Leu5-enkephalin), survived the fixation procedure, and were found to be colocalized throughout the brain. We have observed complex associations between these binding sites and one, two, or all three opioid peptide systems (i.e., proopiomelanocortin, proenkephalin, and prodynorphin) in different brain regions. These multiple opioid peptide-receptor subtype associations are apparent, for example, in neural systems involved in the processing of pain stimuli, and may be important for mediating different types of analgesia. Since differential processing of proenkephalin and prodynorphin can give rise to opioids of varying receptor selectivities, the colocalization of opioid receptor subtypes may signify that such processing is a key regulatory event in determining which receptor subtype is activated and, thus, the physiological consequences of opioid neurotransmission.
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PMID:Anatomical relationship between opioid peptides and receptors in rhesus monkey brain. 615 4

beta endorphin (beta-EP) is an important modulator of central pain pathways. To examine whether changes in central production of beta-EP contribute to the pathogenesis of diabetic neuropathic pain, we compared the cerebrospinal fluid (CSF) levels of beta-EP and its precursor proopiomelanocortin (POMC) between 15 diabetic patients with chronic painful diabetic polyneuropathy, eight patients with severe painless diabetic neuropathy, and ten nondiabetic controls. Both peptides were measured by specific monoclonal antibody-based two-site immunoradiometric assays (IRMAs). In the diabetic patients with painful neuropathy, mean +/- SD CSF beta-EP concentrations (5.7 +/- 2.2 pmol/L) were comparable to those of the diabetic patients with painless neuropathy (6.0 +/- 2.3 pmol/L) and did not correlate with the severity of neuropathic pain. CSF beta-EP, but not POMC, concentrations were lower in the diabetic neuropathic patients overall (5.8 +/- 1.9 pmol/L) compared to the control subjects (7.6 +/- 2.2 pmol/L) (p < 0.05). CSF POMC showed no intergroup differences. However, POMC levels were 80-fold higher than those of beta-EP and should always be considered when interpreting immunoreactive beta-EP or other derivative peptide levels in CSF. We conclude that CSF beta-EP levels appear to be reduced in diabetic polyneuropathy but they do not relate to the presence of neuropathic pain. This might explain why opioid analgesics are of little, if any, help in alleviating diabetic neuropathic pain.
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PMID:Cerebrospinal fluid levels of beta endorphin in painful and painless diabetic polyneuropathy. 759 54

The purpose of this study was to assess whether xenogeneic tumor cells secreting beta-endorphin and immunologically isolated in polymer capsules could survive and continue to reduce pain when transplanted into the spinal cerebro-spinal fluid (CSF) space of rats. Also, a silicone container for polymer capsules was designed for the clinical application of this method of cell therapy. The mouse tumor cell lines, proopiomelanocortin gene transfected Neuro2A which secrete beta-endorphin, were enclosed in polymer capsules at a density of 5 x 10(6)/mL, and transplanted into the spinal CSF space from the occipito-atlantal junction of male Sprague-Dawley rats. Three analgesiometric tests--the tail pinch test, the hot plate test, and electrical stimulation test--showed that the rats with encapsulated Neuro2A (n = 6) were significantly less sensitive to pain after transplantation than control animals (n = 8). The analgesia induced by the encapsulated cells secreting beta-endorphin was attenuated by the opiate antagonist naloxone. Morphological study revealed that the encapsulated cells survived for 1 mo after transplantation into the CSF space. An in vitro experiment on cultured capsules (3 cm long) with a silicone container (Kaneka Medics Co) showed that the encapsulated Neuro2A (5 x 10(6) mL) could secrete peptides for 1 mo. The results of this study indicate that immunologically isolated xenogeneic tumor cells can secrete opiate in the CSF space, and that a silicone container may help the application of this method to the treatment of cancer pain.
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PMID:Cell therapy with encapsulated xenogeneic tumor cells secreting beta-endorphin for treatment of peripheral pain. 779 96

A physiological role for beta-endorphin in endogenous pain inhibition was investigated by targeted mutagenesis of the proopiomelanocortin gene in mouse embryonic stem cells. The tyrosine codon at position 179 of the proopiomelanocortin gene was converted to a premature translational stop codon. The resulting transgenic mice display no overt developmental or behavioral alterations and have a normally functioning hypothalamic-pituitary-adrenal axis. Homozygous transgenic mice with a selective deficiency of beta-endorphin exhibit normal analgesia in response to morphine, indicating the presence of functional mu-opiate receptors. However, these mice lack the opioid (naloxone reversible) analgesia induced by mild swim stress. Mutant mice also display significantly greater nonopioid analgesia in response to cold water swim stress compared with controls and display paradoxical naloxone-induced analgesia. These changes may reflect compensatory upregulation of alternative pain inhibitory mechanisms.
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PMID:Absence of opioid stress-induced analgesia in mice lacking beta-endorphin by site-directed mutagenesis. 863 4


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