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)

Involvement of a central histaminergic mechanism in the stimulating effect of beta-endorphin (beta-End) on the pituitary-adrenocortical activity, measured indirectly through corticosterone secretion, was investigated in conscious rats. The rise in serum corticosterone levels, induced by beta-End injected intraventricularly (icv) was considerably impaired by pretreatment with naltrexone, an opioid receptor antagonist. The stimulating effect of beta-End was almost totally suppressed by a prior icv administration of mepyramine, a histamine H1-receptor antagonist, and also considerably reduced by pretreatment with cimetidine, an H2-receptor antagonist. The strongest suppression, by 83%; of the beta-End-induced corticosterone response was evoked by a prior administration of alpha-fluoromethylhistidine, an inhibitor of neuronal histamine synthesis in the brain. These results indicate that both the brain neuronal histamine and central histamine H1- and H2-receptors are considerably involved in the beta-endorphin-induced stimulation of the pituitary-adrenocortical activity.
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PMID:The influence of alpha-fluoromethylhistidine and histamine receptor antagonists on the beta-endorphin-induced corticosterone response. 200 50

alpha N-acetyl human beta-endorphin-(1-31) injected icv to mice antagonized the analgesic activity of beta-endorphin-(1-31) and morphine whereas the analgesia evoked by DADLE and DAGO was enhanced by this treatment. The modulatory activity of alpha N-acetyl beta-endorphin-(1-31) was exhibited at remarkable low doses (fmols) reaching a maximum that persisted even though the dose was increased 100,000 times. The regulatory effect of a single dose of the acetylated neuropeptide lasted for 24h. The activity of alpha N-acetyl human beta-endorphin-(1-31) was partially retained by the shorter peptide alpha N-acetyl human beta-endorphin-(1-27) and to a lesser extent by beta-endorphin-(1-27), beta-endorphin-(1-31) lacked this regulatory activity on opioid analgesia. Acetylated beta-endorphin-(1-31) displayed a biphasic curve when competing with 5 pM [125I]-Tyr27 human beta-endorphin-(1-31) specific binding, the first step (20 to 30% of the binding) was abolished with an apparent IC50 of 0.35 nM, and the rest with an IC50 of 200 nM. It is suggested that alpha N-acetyl beta-endorphin-(1-31) changed the efficiency of the opioid analgesics by acting upon a specific substrate that is functionally coupled to the opioid receptor, presumably the guanine nucleotide binding regulatory proteins Gi/Go.
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PMID:alpha N-acetyl derivatives of beta-endorphin-(1-31) and -(1-27) regulate the supraspinal antinociceptive activity of different opioids in mice. 200 58

We have previously shown that central administration of beta-endorphin results in a reduction of ornithine decarboxylase activity. Ornithine decarboxylase catalyses the rate-limiting step in the biosynthesis of the polyamines putrescine, spermidine and spermine, thought to modulate nucleic acid synthesis. The present study examines the effects of intracisternal injection of beta-endorphin on brain and liver DNA synthesis in preweanling rats. In six-day-old rats, beta-endorphin (0.75 micrograms/g brain wt) produced approximately a 70% inhibition in brain and liver DNA synthesis 1 h after injection, and values were still subnormal in both tissues 10 h later. Subcutaneous administration of beta-endorphin did not alter liver DNA synthesis. Thus, it is most likely that the suppressed liver DNA synthesis observed in animals given beta-endorphin intracisternally is mediated by central mechanisms. Co-administration of naloxone plus beta-endorphin intracisternally prevented the response, indicating an opioid receptor-mediated phenomenon. Naloxone alone caused small but significant increases in brain and liver DNA synthesis, suggesting a tonic influence on tissue DNA by endogenous opioids in the CNS. Acute inhibition of ornithine decarboxylase activity by alpha-difluoromethylornithine did not alter DNA synthesis, indicating that the decreases in DNA synthesis induced by beta-endorphin are unrelated to the ornithine decarboxylase/polyamine system. The effect appears to be restricted to early development as no significant changes in DNA synthesis were obtained in 20-day-old animals. The results from these studies indicate that CNS beta-endorphin has the ability to influence DNA synthesis in central as well as in peripheral tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of central administration of beta-endorphin on brain and liver DNA synthesis in preweanling rats. 205 54

We have examined in vitro the effect of the proopiomelanocortin gene product, beta-endorphin (bE), on the cytotoxic activity of natural killer (NK) cells, lymphokine activated killer (LAK) cells and cytotoxic T-lymphocytes (CTL). Our studies show that bE reproducibly suppressed LAK cytotoxic activity in all donors tested. The effect of bE on the generation of CTL varied, and was negligible on CTL cytotoxic function. Our study also confirms the variable nature of the effects of bE on NK cytotoxicity. In all instances, the effects of bE were generally small, but could be blocked by opioid receptor antagonists, or by prior heat-inactivation of the peptide. The magnitude of the effects was greatest at low effector:target ratios in all of the three systems studied. These results support the emerging body of evidence that the neuroendocrine system may influence host defense mechanisms mediated by cytotoxic cells.
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PMID:Differential effect of beta-endorphin on three human cytotoxic cell populations. 207 1

Previous studies have demonstrated that abolition of the naloxone-stimulated increase in plasma LH levels is characteristic of hypothalamic dysfunction in experimental uremia. This study aimed to further characterize the nature of the defect in hypothalamic opiatergic mechanisms in experimental uremia. Specifically, we have tested the hypothesis that naloxone resistance was due to either opioid receptor dysfunction or diminished opioid peptide levels. Administration of naloxone (2 mg/kg, iv) to cannulated freely mobile rats confirmed previous observations that despite marked increases in plasma LH in control rats, plasma LH levels were unaffected in uremic male rats (P = 0.001 for group x time interaction). In a second experiment, morphine (2 mg/kg) or saline diluent was given quasi-continuously as small aliquots before each blood sample during the pulse studies of castrate mature male rats that had undergone either subtotal nephrectomy or sham operation. After the administration of morphine, uremic rats exhibited a 60% reduction in mean LH levels (14.9 +/- 1.4 vs. 6.0 +/- 0.7 ng/ml) attributable to a 42% reduction in LH pulse frequency (3.6 +/- 0.4 vs. 2.1 +/- 0.5 peaks/3 h) and a 60% reduction in LH pulse amplitude (4.7 +/- 0.5 vs. 1.9 +/- 0.3 ng/ml). The preservation of sensitivity to morphine despite complete naloxone resistance raised the alternate hypothesis of depletion of endogenous opiate peptide levels in the uremic hypothalamus. This hypothesis was tested by measuring the beta-endorphin content of the medial basal hypothalamus (MBH) in a rat beta-endorphin RIA. Rat MBH beta-endorphin content was not significantly altered specifically by either uremia or castration. We conclude, therefore, that naloxone resistance of plasma LH in experimental uremia is not due to either defects in opioid receptor function or reduced hypothalamic beta-endorphin content. Instead, we suggest that uremia may diminish the release of endogenous opioid peptides that interact with GnRH neurons from the MBH.
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PMID:Hypothalamic opioid mechanisms in experimental uremic hypogonadism. 213 74

1. Intraventricular administration of human beta-endorphin and elephant beta-endorphin significantly prolonged the tail flick response tested 30 min later. However, elephant beta-endorphin was about 7-8 times more potent than human beta-endorphin in the tail flick test. 2. beta-Endorphin antagonized the antinociceptive effect of both human beta-endorphin and elephant beta-endorphin by the same extent. Naloxone also antagonized the antinociceptive effects of the beta-endorphins but it was less effective than beta-endorphin. 3. Human beta-endorphin and elephant beta-endorphin were of equal potency in inhibiting the abdominal constriction response induced by intraperitoneal (i.p.) acetic acid. Both beta-endorphin and naloxone antagonized these effects of the beta-endorphins with naloxone being more effective. 4. The present study showed that different opioid receptor subtypes may be involved in the tail flick test and the abdominal constriction test. Furthermore, elephant beta-endorphin was a better antinociceptive agent than human beta-endorphin in the tail flick test.
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PMID:Preliminary study on the antinociceptive effect of elephant beta-endorphin. 214 Sep 62

It has been shown that opioid peptides induce histamine release and enhance antigen-induced histamine release from isolated peritoneal mast cells. Little is known about the effect of opioid peptides on mast cells present in airway smooth muscle. In the present study, the effect of beta-endorphin on antigen-induced contractions of isolated tracheal rings from actively sensitized guinea pigs was studied. It appears that beta-endorphin has a bidirectional effect on anaphylactic contractions of the trachea. Low concentrations of beta-endorphin (0.1 and 10 nM) significantly potentiate the anaphylactic contractions of tracheal rings. In contrast, higher concentrations of beta-endorphin (0.1 and 1 microM) significantly suppress the anaphylactic contractions of guinea pig trachea. In the presence of the non-selective opioid receptor antagonist naloxone, 10 nM of beta-endorphin still potentiates the anaphylactic contractions of the trachea. This demonstrates that the potentiation of anaphylactic contractions of guinea pig trachea by low concentrations of beta-endorphin is not mediated by opioid receptors. We speculate that the potentiation of the anaphylactic contraction by beta-endorphin is due to an interaction with mast cells.
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PMID:Beta-endorphin modulates anaphylactic contractions of tracheae isolated from actively sensitized guinea pigs. 214 66

Antinociceptive tolerance and cross-tolerance to intracerebroventricular (i.c.v.) beta-endorphin, morphine, and DPDPE (D-Pen2-D-Pen5-enkephalin) induced by a prior i.c.v. administration of beta-endorphin, morphine and DPDPE, respectively, were studied in mice. Acute tolerance was induced by i.c.v. pretreatment with beta-endorphin (0.58 nmol), morphine (6 nmol) and DPDPE (31 nmol) for 120, 180 and 75 min, respectively. Various doses of beta-endorphin, morphine or DPDPE were then injected. The tail-flick and hot-plate tests were used as antinociceptive tests. Pretreatment of mice with beta-endorphin i.c.v. reduced inhibition of the tail-flick and hot-plate responses to i.c.v. administered beta-endorphin, but not morphine and DPDPE. Pretreatment of mice with morphine i.c.v. reduced inhibition of the tail-flick and hot-plate responses to morphine but not beta-endorphin. Pretreatment of mice with DPDPE reduced inhibition of the tail-flick and hot-plate responses to DPDPE but not beta-endorphin. The results indicate that one injection of beta-endorphin, morphine or DPDPE induces acute antinociceptive tolerance to its own distinctive opioid receptor and does not induce cross-tolerance to other opioid agonists with different opioid receptor specificities. The data support the hypothesis that beta-endorphin, morphine and DPDPE produce antinociception by stimulating specific epsilon, mu- and delta-opioid receptors, respectively.
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PMID:Lack of antinociceptive cross-tolerance between intracerebroventricularly administered beta-endorphin and morphine or DPDPE in mice. 215 19

Overnight treatment of murine leukocytes with corticotropin-releasing hormone (CRH) and arginine vasopressin enhances natural killer cell activity. Moreover, the opioid receptor antagonist, naloxone, as well as the delta-class opioid receptor antagonist, naltrindole, can block this effect. The responsivity of murine leukocytes to CRH is both dose- and time-dependent. The effector cells are both MAC-1 and Thy-1.2 antigen-positive. Whereas beta-endorphin is also shown to enhance natural killer cell activity in a naloxone-reversible manner, adrenocorticotropic hormone (ACTH) has a negligible effect. Macrophage depletion prior to incubation with CRH blocks the CRH-induced natural killer cell augmentation. These results suggest hypothalamic-releasing hormones such as CRH may have a biologically relevant role in the modulation of immune cells either directly or indirectly through the induction of neuropeptide hormones known to have immunomodulatory capabilities.
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PMID:Corticotropin-releasing hormone augments natural killer cell activity through a naloxone-sensitive pathway. 216 Apr 75

Male ICR mice were rendered tolerant by intrathecal (IT) injection once a day with either mu-agonist, D-Ala2-NMePhe4-Gly-ol-enkephalin (DAMGO) or delta-agonist, D-Pen2-D-Pen5-enkephalin (DPDPE) (toleragen) by doubling the dose each day starting from 0.125 and 1 microgram for DAMGO and DPDPE, respectively, for 6 days. On day 6, the magnitude of tolerance was assessed by establishing IT dose-response lines for the effect of the chronic drug given as bolus injections (probe). The antinociception was assessed by the tail-flick and hot-plate test. Repeated IT injections of DPDPE reduced inhibition of the tail-flick and hot-plate response induced by DPDPE (ED50 values for DPDPE increase 10-fold) but not DAMGO. Repeated IT injections of DAMGO reduced inhibition of the tail-flick and hot-plate response induced by DAMGO (ED50 value for DAMGO increase 7- to 10-fold) but not DPDPE. The effects of the tolerance to mu- and delta-opioid receptor activity in the spinal cord on inhibition of the tail-flick and hot-plate response induced by intracerebroventricularly (ICV) administered beta-endorphin and morphine were then studied. beta-Endorphin or morphine at different doses were injected ICV 4 hr after the last IT injection of DPDPE or DAMGO. Repeated IT bolus injections of DPDPE reduced inhibition of the tail-flick response but not the hot-plate response induced by beta-endorphin. On the other hand, repeated IT bolus injections of DAMGO did not affect inhibition of the tail-flick and hot-plate response induced by beta-endorphin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tolerance to delta- but not mu-opioid receptors in the spinal cord attenuates inhibition of the tail-flick response induced by beta-endorphin administered intracerebroventricularly in mice. 216 Nov 7


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