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)

In several diseases chronic pain is associated with long-lasting pathophysiological responses which differ strongly from those observed in acute situations. When persisting, acute pain often results in physical and psychological stress which may in turn aggravate the initial pathological state. In the present work we examined the secretory patterns of pituitary hormones related to acute stress (growth hormone (GH), prolactin (PRL) and beta-endorphin (beta-END)) in rats during the phase of Freund adjuvant-induced arthritis (AIA, a model used for chronic pain studies) when chronic pain is maximum (14 and 21 days, postinoculation (PI)). Using radio-immunoassay hormones were measured in plasma samples taken every 30 min for 7 h in free-moving rats 14 and 21 days after Freund adjuvant or vehicle injection and in control animals. The total amount of GH secretion was higher at 14 and 21 days PI in AIA rats as compared to vehicle-treated and control animals, and the pulsatility of GH secretory pattern was not modified by AIA. PRL and beta-END secretion were not significantly different in arthritic rats as compared to controls. These results show that GH, PRL and beta-END responses induced by acute stress are not observed during the AIA phase when chronic pain is maximum. Thus, in our experimental conditions, beta-END and PRL do not seem to be good plasma markers of chronic pain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic pain induces a paradoxical increase in growth hormone secretion without affecting other hormones related to acute stress in the rat. 159 79

Discovery of the endogenous opiate system of the brain has revolutionized the study of pain and pain management. In this study a convenience sample of 10 pregnant women, 16 nonpregnant women, and 18 men were studied to determine if changes in plasma beta-endorphin-like immunoreactivity affected pain perception during labor. Pregnant women had plasma levels of beta-endorphin significantly higher than nonpregnant women at the midpoint of their menstrual cycle, t = 3.74, df = 31, p = .007. Self-reported pain perception scores were not correlated with plasma beta-endorphin levels. However, as labor progressed, the women reported increased discomfort between contractions and during contractions while beta-endorphin levels increased only slightly. Close examination of the pain pattern indicates that pain perceived by the women between contractions increased at a greater rate than during contractions. This pattern suggests that opiate-active beta-endorphin may increase the ability of women to tolerate acute pain.
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PMID:Beta-endorphin levels during pregnancy and labor: a role in pain modulation? 252 22

The concentrations of endogenous opiates (beta-endorphin, methionine-enkephalin, leucine-enkephalin) in the spinal fluid and arterial blood plasma has been studied in 16 dogs, using the model of acute pain stimulation under electroacupuncture analgesia (EAA). It has been shown that pain stimulation under EAA is accompanied by a significant increase in methionine-enkephalin++ and leucine-enkephalin concentrations (by 244 and 69.4%, respectively) in the spinal fluid. beta-endorphin level tends to increase. There is also a trend towards the reduction in beta-endorphin and methionine-enkephalin concentrations in the arterial blood plasma, which is indicative of effective antinociceptive stimulation of the endogenous opiate system. However, by the end of the first hour a decrease of methionine-enkephalin and leucine-enkephalin levels in the spinal fluid was paralleled by a trend towards beta-endorphin and methionine-enkephalin increase and a significant leucine-enkephalin increase in arterial blood plasma, which can account for the exhaustion of the opiate system.
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PMID:[Changes in the concentration of endogenous opiates in the blood and cerebrospinal fluid during acute painful stimuli and protective electroacupuncture analgesia]. 262 35

Certain neuropeptides previously linked to stress and implicated in CNS control of analgesia/algesia were tested using a recently developed analgesiometric model, the rabbit ear-withdrawal test. The latency to ear withdrawal increased in a dose-related manner after beta-endorphin was injected intracerebroventricularly (IVC). Intermediate doses (0.5 and 1.0 micrograms) of adrenocorticotropic hormone (ACTH) caused hyperalgesia as indicated by decreases in latency. Corticotropin-releasing factor (CRF, 0.5 and 1.0 micrograms) also caused significant hyperalgesia late in the testing period. alpha-Melanocyte stimulating hormone (alpha-MSH, 0.25-2.0 micrograms), a molecule that shares the first 13 amino acid sequence with ACTH, and somatostatin (0.25-2.0 micrograms), caused no significant change in latency. However, 1.0 microgram doses of each peptide antagonized the analgesic effect of beta-endorphin (1.0 microgram) in the following order of potency: ACTH = alpha-MSH greater than CRF greater than somatostatin. The results support the idea that CNS peptides that are released during stress can exert opposing actions on acute pain, even though they may cause little effect alone.
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PMID:Influence of centrally administered peptides on ear withdrawal from heat in the rabbit. 288 94

Patients with chronic low-back pain and depression were treated double blind with desipramine or doxepin. During this treatment several hypotheses regarding the modes of action of these drugs were examined. A low serotonin hypothesis was supported by the fact that patients who had pain relief following an acute challenge with fenfluramine, a relatively pure releaser of serotonin, were significantly more likely to have pain relief on either antidepressant. The antidepressants did not change cerebrospinal fluid (CSF) beta-endorphin levels, acute pain tolerance, or electromyogram (EMG) levels. The nonsedating antidepressant desipramine was as effective as doxepin; 60% of patients had significant pain relief. Pain relief was associated with depression relief, but several patients had only pain or depression relief. Patients who had a substantial physical basis for their pain responded as well as those who did not.
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PMID:Tricyclic antidepressants for chronic low-back pain. Mechanisms of action and predictors of response. 294 34

Due to recent interest in the development of drug assay techniques, the pharmacokinetics of many analgesics have been defined. In addition, mechanisms of action of the commonly used analgesics have been partly delineated, and currently accepted analgesic regimens and usages are being questioned. By considering both the pharmacokinetics and the mechanism of action of each of these analgesics, it would appear that only a few of the currently available agents are needed for the treatment of acute and chronic pain. Newer agents with reduced toxicity have been introduced but have resulted in little expansion of novel ways to interfere with pain. The recent discovery of the beta-endorphin system, the reevaluation of older agents, and the development of new agents that work at pain pathways other than the classical sites hold out the promise of alternative means of control of certain types of pain. An agent that has analgesic efficacy equivalent to morphine but with reduced toxicity is especially exciting in the development of new analgesics. An agent that, in addition, does not lead to intolerable psychomimetic reactions but instead addresses multiple aspects of treating the fear, pain, and tension triad of pain will be beneficial in acute pain but will especially enhance the spectrum of the control of chronic pain such as cancer, neuralgia and arthralgia.
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PMID:Pharmacokinetics and mechanisms of action of analgesics in clinical pain. 611 74

Since the discovery of the link between peripheral endogenous opioid peptides and pain regulation, these substances have been studied in relation to certain pain conditions. In order to elucidate the effect of chronic pain on both peripheral opioid system and sympathetic nervous activity, we assayed plasma met-enkephalin (ME), neutrophil met-enkephalin containing peptides (NMECP) and plasma free and conjugated catecholamines (CA) in lung cancer patients with chronic pain related to bone metastases and without pain. No significant difference was found in ME levels when the pain cancer group (0.36 +/- 0.06 pmol/ml) was compared to the pain-free group (0.37 +/- 0.04 pmol/ml); results were similar for NMECP levels (14.1 +/- 1.66 pmol/mg prot and 18.41 +/- 1.93 pmol/mg prot, respectively). CA levels in both groups were also similar. These results differ from those we have reported previously for acute pain, suggesting that a non-permanent painful stimulus may be necessary for peripheral opioid system stimulation.
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PMID:Lack of response of proenkephalin A and sympathetic nervous system in chronic pain associated with lung cancer. 808 50

The transplantation of cells that secrete neuroactive substances with analgesic properties into the CNS is a novel method that challenges current approaches in treating chronic pain. This review covers pre-clinical and clinical studies from both allogeneic and xenogeneic sources. One cell source that has been utilized successfully is the adrenal chromaffin cell, since such cells constitutively release catecholamines, opioid peptides, and neurotrophic factors; release can be augmented with nicotine. Other graft sources include AtT-20 and B-16 cell lines which release enkephalins and catecholamines, respectively. For grafting in rodents, adrenal medullary tissue pieces are transplanted to the subarachnoid space. Chromaffin cell transplants can decrease pain sensitivity in normal rats using standard acute pain tests (paw-pinch, hot-plate, and tail-flick). In addition, transplants can restore normal pain thresholds in rodent models of chronic pain (formalin, adjuvant-induced arthritis, and sciatic-nerve tie) which closely similate the pathologies of human chronic pain conditions. Xenografts have been studied due to concerns that future application for human pain may be limited by donor availability. Despite immune privileges of the CNS, xenografts require at least short-term immunosuppression to obtain a viable graft. Cell encapsulation is one method of sustaining a xenograft (in rat and human hosts) while circumventing the need for immunosuppression. Clinical studies have been initiated for terminal cancer patients with promising results as assessed by markedly reduced narcotic intake, visual analog scale ratings, and increased CSF levels of catecholamines and met-enkephalin.
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PMID:Update on cellular transplantation into the CNS as a novel therapy for chronic pain. 853 50

The influence of anxiety on acute pain sensation was investigated, studying the relative contribution of endogenous opioids and attentional mechanisms. Thirty-six spider phobics received mildly painful electrical stimulation, while anxiety and focus of attention were manipulated within subjects. The opioid antagonist naloxone or placebo was administered between subjects to examine an analgesia owing to anxiety-induced endorphinergic activity. In contrast to earlier findings, attention towards pain failed to increase pain as opposed to distraction from pain, probably owing to a less effective attention manipulation. Furthermore, despite high levels of anxiety, subjective pain ratings were not influenced by anxiety, although heart rate responses were slightly inhibited. Accordingly, there was no increase in subjective or physiological pain responses as a result of naloxone, nor did beta-endorphin plasma levels rise during anxiety. The results suggest that phobic anxiety does not induce an opioid-mediated analgesia. Curiously, naloxone itself effected a dose-dependent analgesia compared to placebo during both high and low anxiety, which is compatible with the assumption of agonist properties of naloxone in the absence of opioid activity.
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PMID:No evidence for opioid-mediated analgesia induced by phobic fear. 929 2

Clients report more pain at some times of day than at others due, in part, to the temporal variation of the body's inhibitory pain response. The analgesic effectiveness of morphine varies with the time of day, perhaps due to the inhibiting or enhancing effects of the drug on plasma beta-endorphin (BE). This experiment was designed to examine the timed effects of morphine on the pain-induced BE response. Six groups of treatment mice (injected with morphine sulfate) and 6 groups of control mice (injected with saline) were exposed to an acute pain stimulus at 4-h intervals, and blood was collected. Plasma BE was analyzed using radioimmunoassay. Control mice showed a robust circadian BE-response rhythm with a peak at 0000 and a nadir at 1200, whereas the BE response of mice that received morphine was arrhythmic. Animals that received morphine tolerated the noxious stimulus longer, but the analgesia varied with time of day. These results indicate that morphine abolishes the rhythmic BE response to pain and does not inhibit pain equally at all times of day. Morphine doses should be titrated to maximize the endogenous pain control system while achieving analgesia with decreased dosages.
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PMID:Effects of morphine and time of day on pain and beta-endorphin. 1453 Dec 15


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