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)

A seventeen year old boy presented with destructive arthropathy of the lower limbs and discovertebral spaces. Past history yielded recurrent episodes of indolent fractures and progressive knee and ankle deterioration. The patient denied any pain sensation in the past and at examination. Other neurological tests were normal. Beta-endorphin level was elevated in the CSF. Response to the cold pressor test was modified after injection of Naloxone. The nosology and physiopathology of congenital insensitivity to pain are discussed.
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PMID:[A case of congenital insensitivity to pain with destructive arthropathies of the limbs and spine. Discussion on nosology and physiopathology of the disease]. 242 25

Pain sensitivity of food and/or water-deprived male mice was tested on a hotplate. The most pronounced analgesia ensued in animals given no food and water, and no food but water ad libitum, the least one in water-deprived mice. The magnitude of the rise in pain threshold depended on the duration of deprivation and was correlated with the increase in the blood plasma beta-endorphin level. In the hypothalamus beta-endorphin level increased after 72-h food deprivation only. The level of dynorphin remained unchanged. Naloxone (10 mg/kg) almost completely reversed food or water-deprivation induced analgesia.
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PMID:The effect of food and water deprivation on post-stress analgesia in mice and levels of beta-endorphin and dynorphin in blood plasma and hypothalamus. 242 64

Pressor (VLPA) and depressor (VLDA) areas of the ventrolateral medulla were identified by microinjections of L-glutamate in urethane-anesthetized rats. Cardiovascular effects of opiate agonists microinjected into the same sites were then studied. Agents used to stimulate mu, delta, sigma, kappa, and beta-endorphin (epsilon) receptors were morphiceptin, D-Ala2-D-Leu5-enkephalin, N-allyl-normetazocine, dynorphin, and beta-endorphin, respectively. Opiate receptor stimulation in VLPA decreased blood pressure (BP) and heart rate (HR), while in VLDA it increased BP and HR. Thus, it is the site of injection rather than the type of opiate receptor that determines cardiovascular responses. Naloxone, an opiate antagonist, reversed and prevented these responses. Abolition of cardiovascular responses by spinal transection at the C1 level indicated that the sympathetic nervous system mediated these responses. The following mechanism is proposed for these actions of opiates: Cell bodies in VLPA, but not in VLDA, project to the intermediolateral cell column of the spinal cord. Opiates inhibit VLPA and lower BP and HR by decreasing sympathetic outflow. Opiate-induced inhibition of VLDA, which has an inhibitory effect on VLPA, results in an increase in BP and HR.
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PMID:Cardiovascular responses to medullary microinjections of opiate agonists in urethane-anesthetized rats. 242 96

Spontaneously elevated nociceptive threshold levels were markedly diminished after Naloxone injections in 4 patients with congenital insensitivity to pain. This finding suggested the hypothesis of a relation between congenital insensitivity to pain and permanent hyperfunction of an endomorphinic system. Radio-immunoassay of CSF beta-endorphin was performed in all 4 cases. The normal or only slightly elevated levels cannot explain electrophysiologic findings, but as a function of the multiplicity of endogenous opioid systems, hyperactivity of another endomorphinic system cannot be excluded. Other hypotheses may also be proposed.
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PMID:[Cerebrospinal fluid beta-endorphin in congenital insensitivity to pain]. 243 47

The pathophysiological consequences of endorphin release in anaphylactic shock were investigated through pharmacological studies using opiate antagonists (naloxone, naltrexone, natrexone methyl bromide) as well as agonists (morphine, beta-endorphin). These studies suggest that induction of anaphylaxis provokes the release of endogenous opioids, possibly from the hypothalamus, which contribute to the shock process by stimulating opiate receptors in the CNS. The mechanism of pathophysiologic action of endorphin in anaphylaxis involves, at least in part, inhibition of the central component of the sympatho-adrenalmedullary system. This results in reduced effectiveness of the sympathetic system to physiologically reverse the circulatory effects of the toxic mediators of anaphylaxis. Naloxone, by blocking endorphin action at CNS opiate receptors located at autonomic regulatory centers (e.g. hypothalamus), reverses the sympatho-inhibitory effect of the endorphin peptides. This results in increased central sympathetic outflow to peripheral sympathetic neuroeffector mechanisms; it affords improved sympathetic compensatory responses and increases survival. TRH and DT gamma E physiologically oppose the action of endorphins upon the autonomic system. They stimulate central sympathetic mechanisms through their own receptor systems and increase outflow to peripheral sympathetic effectors. This also results in improved circulatory function and survival.
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PMID:Anaphylactic shock: catecholamine actions in the responses to opioid antagonists. 245 93

An in vitro model system for analysis of presynaptic inhibitory actions of spinal opioids has been applied. Embryonic sensory neurons derived from chick dorsal root ganglia were grown in primary cell culture, and the release of substance P was evoked by electrical field stimulation during exposure to drugs with well-demonstrated affinity for opioid receptors. This allowed a pharmacologic characterization of the inhibitory actions of specific opioid agonists on the release of substance P as measured by radioimmunoassay (RIA). Sufentanil (0.5 microM), a high affinity mu receptor agonist, U-50,488H (25 microM), a selective kappa receptor agonist, and morphine (10 microM), an agonist with high affinity for mu and delta receptors, inhibited the evoked release of substance P by approximately 60%, 40%, and 50%, respectively. For sufentanil the response was demonstrated to be dose-dependent. As is the case for its analgesic action in vivo, morphine was approximately 50-fold less potent than sufentanil on a molar basis in this assay. The actions of sufentanil, U-50-488H and morphine were mimicked by the endogenous opioid peptide met-enkephalin, and its stable synthetic analog D-ala2-met5-enkephalinamide (DAME). Naloxone (25 microM), an opioid receptor antagonist, blocked the inhibitory action of sufentanil (0.5 microM), morphine (5 microM), and DAME (5 microM), but not U-50,488H (10 microM). The action of U-50,488H was partially blocked by the antagonist naltrexone (25 microM). Stereo-selectivity of agonist action was confirmed by the failure of dextrorphan (50 microM), an inactive opioid isomer, to inhibit the release of substance P.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sufentanil, morphine, met-enkephalin, and kappa-agonist (U-50,488H) inhibit substance P release from primary sensory neurons: a model for presynaptic spinal opioid actions. 246 89

Rat peritoneal mast cells were exposed to the neurohormone and basic opioid peptide beta-endorphin. beta-Endorphin induced a dose-dependent release of histamine from the mast cells. A significant histamine release was found at 5 mumol/l of beta-endorphin and maximal release (35% of total) at 20 mumol/l. The histamine release process was very rapid and terminated within 30 s at 37 C, and in this sense is very similar to the histamine release induced by compound 48/80 or neurotensin. The histamine release was temperature-dependent showing an optimum release around 30 C, and it was independent of available extracellular calcium, but was inhibited in the presence of high extracellular calcium concentrations. Naloxone, only in very high concentrations (10 mmol/l), inhibited the release, and the very same concentration also inhibited the neurotensin - as well as the compound 48/80-induced histamine release. Cromoglycate and benzalkoniumchloride, a 48/80 antagonist, both produced a progressive dose-dependent inhibition of beta-endorphin-, neurotensin- as well as compound 48/80-induced histamine release. Taken together, the findings indicate that the opioid peptide beta-endorphin induces a selective, energy-dependent release of histamine from peritoneal rat mast cells. The pattern of release has much in common with that of compound 48/80 and other basic peptides, such as neurotensin and substance P. In addition this pattern of release is similar to that induced by dynorphin.
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PMID:Characteristics of beta-endorphin-induced histamine release from rat serosal mast cells. Comparison with neurotensin, dynorphin and compound 48/80. 246 22

The supraoptic nucleus of male and female rats treated with met-enkephalin or naloxone and met-enkephalin was examined with light microscopical immunocytochemistry for Arginine-vasopressin. Both genders exhibited the same distribution of immunostained magnocellular neurons. Met-enkephalin treatment caused an increase in number of immunostained vasopressin neurons. This effect was more pronounced in females than in males. Naloxone treatment diminished immunoreactive cytoplasmic vasopressin in males more effectively than in females. In enkephalin-treated animals numerous vasopressin immunoreactive varicosities appeared within the supraoptic nucleus, but were mostly absent in naloxone-treated animals and in controls. Our results indicate that met-enkephalin treatment either stimulates vasopressin synthesis or inhibits secretion. It is likely that steroid hormones mediate the action of enkephalin on vasopressin secretion in a specific manner.
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PMID:Sex-specific effects of met-enkephalin treatment on vasopressin immunoreactivity in the rat supraoptic nucleus. 247 72

Intravenous administration of small doses of beta-endorphin causes immediate suppression of basal and glucose-stimulated insulin secretion in normal rabbits. The purpose of the present study was to determine if beta-endorphin directly inhibits glucose-stimulated insulin secretion from rabbit pancreatic islets. Islets were isolated from male New Zealand White rabbits and perifused for 1 h with medium containing 100 mg/dl glucose (M100) followed by a 1-h challenge with medium containing 300 mg/dl glucose (M300) with or without beta-endorphin and/or the specific opioid antagonist naloxone. Samples were collected every 5 min during the last 30 min of the baseline perifusion with M100 and during the 1-h challenge with the stimulatory concentration of glucose (M300). Total insulin secretion for each 1-h period was calculated by adding the areas under the curves for twice the 30-min baseline period and for the 1-h challenge period. The mean +/- SE area for the control islets during perifusion with M100 was 5.9 +/- 0.8 microU/islet.h. M300 stimulated a 4.2-fold increase in the amount of insulin secreted (24.5 +/- 3.6 microU/islet.h). The stimulated rate of insulin release was sustained throughout the 1-h test period with M300, averaging 0.42 +/- 0.02 microU insulin/islet.min. beta-Endorphin inhibited glucose-stimulated insulin secretion in a concentration-dependent manner. Maximal suppression of insulin secretion to a level well below the baseline secretion rate was produced by 300 nM beta-endorphin (1.9 +/- 0.3 microU/islet.h). The first 15 min of glucose-stimulated insulin secretion was 6 times less sensitive to the inhibitory effect of beta-endorphin than was the next 45 min. The concentrations of beta-endorphin causing 50% inhibition of glucose-stimulated insulin secretion (IC50) for the 5- to 15-, 20- to 60-, and 5- to 60-min intervals were 1.96, 0.35, and 0.57 nM, respectively. Naloxone (3 microM) had no effect on glucose-stimulated insulin secretion, but partially antagonized the inhibitory effect of 30 nM beta-endorphin (10.2 +/- 2.9 microU/islet.h naloxone plus beta-endorphin vs. 2.6 +/- 1.1 microU/islet.h beta-endorphin; P less than 0.05). These data demonstrate that beta-endorphin, at low concentrations, has a direct inhibitory effect on insulin secretion, and they support the idea that a naloxone-sensitive beta-endorphin-binding component is present in pancreatic islets.
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PMID:Beta-endorphin inhibits insulin secretion from isolated pancreatic islets. 252 21

Microiontophoretic application of beta-endorphin activated neuronal activity (48%) rather than inhibited it (38%) or had no effect whatsoever (14%) in the later hypothalamus of satiated rabbits. Naloxone inhibited the neuronal activity in 75% of the cases as well as activated it (25%), no areactive neurons having been found. The variations of latency of the interspike intervals due to the effect of beta-endorphin depended on the background activity of the neurons. The beta-endorphin--sensitive neurons seem to play a part both in neuronal mechanisms of feeding motivation and in those of satiation.
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PMID:[Participation of beta-endorphins in organizing neuronal activity of the rabbit hypothalamic "hunger centers"]. 252 99


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