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)

Intraventricular injection of beta-endorphin (3, 7, 10 and 30 nmol/kg) into the third ventricular of pentobarbital-anaesthetized male Sprague-Dawley rats resulted in a dose-dependent increase in mean arterial pressure (MAP) while injection of the same volume of 0.9% NaCl solution did not cause significant changes in MAP. Naloxone, which did not produce any significant change in MAP, antagonized the vasopressor effect of beta-endorphin, indicating that the response is mediated via the naloxone sensitive opiate receptors. Rats acclimated to cold (5 degrees) for 3 weeks showed a potentiated and prolonged increase in MAP following beta-endorphin injection, indicating an increased responsiveness to the peptide. This increased responsiveness in the cardiovascular system is probably of adaptive value in cold acclimation. Naloxone itself did not alter MAP either, but abolished the cardiovascular response to beta-endorphin completely in cold acclimated rats, indicating an increased effectiveness in its antagonistic effect following cold acclimation as well.
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PMID:Cold acclimation increases physiological responsiveness to intraventricular injection of beta-endorphin in pentobarbital anaesthetized rats. 1. Cardiovascular functions. 632 48

The effects of intense exercise on pain perception, mood, and plasma endocrine levels in man were studied under naloxone and saline conditions. Twelve long-distance runners (mean weekly mileage = 41.5) were evaluated on thermal, ischemic, and cold pressor pain tests and on mood visual analogue scales (VAS). Blood was drawn for determination of plasma levels of beta-endorphin-like immunoreactivity (BEir), growth hormone (GH), adrenocorticotrophic hormone (ACTH), and prolactin (PRL). These procedures were undertaken before and after a 6.3 mile run at 85% of maximal aerobic capacity. Subjects participated on two occasions in a double-blind procedure counterbalanced for drug order: on one day they received 2 i.v. injections of naloxone (0.8 mg in 2 ml vehicle each) at 20 min intervals following the run; on the other day, 2 equal volume injections of normal saline (2 ml). Sensory decision theory analysis of the responses to thermal stimulation showed that discriminability, P(A), was significantly reduced post-run under the saline condition, a hypoalgesic effect; response bias, B, was unaffected. Ischemic pain reports were significantly reduced post-run on the saline day, also a hypoalgesic effect. Naloxone reversed the post-run ischemic but not thermal hypoalgesic effects. Joy, euphoria, cooperation, and conscientiousness VAS ratings were elevated post-run; naloxone attenuated the elevation of joy and euphoria ratings only. Plasma levels of BEir, ACTH, GH, and PRL were significantly increased post-run. The results show that long-distance running produces hypoalgesia and mood elevation in man. The effects of naloxone implicate endogenous opioid neural systems as mechanisms of some but not all of the run-induced alterations in mood and pain perception.
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PMID:Pain sensitivity, mood and plasma endocrine levels in man following long-distance running: effects of naloxone. 633 Jun 43

Analgesia induced in rats by cold-water swim stress and measured by the tail-flick and hot-plate methods was significantly antagonized after IP pretreatment for 3 days with 8 mg/kg dexamethasone. The analgesia developed by the cold-water swim stressor was also attenuated by 1 mg/kg naloxone. These results suggest that the corticosteroids may have a role in modulating stress-induced analgesia and that the adrenal-pituitary axis modulates the endogenous opiate system. These conclusions are based on recent reports that indicate the release of the opiate-like peptide beta-endorphin and adrenocorticotropin (ACTH) from the pituitary are increased by acute stress and inhibited by administration of the synthetic glucocorticoid dexamethasone.
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PMID:Dexamethasone and stress-induced analgesia. 640 29

The actions of classical neurotransmitters at the synapse are rapidly terminated either by re-uptake or by enzymatic degradation. Enkephalins, like other neurotransmitters, have been demonstrated to be degraded by active proteinases present in the brain. However, it has been generally assumed that an uptake process is not operant for met-enkephalin. To confirm or disprove this assumption, we examined the problem of met-enkephalin uptake in rat brain synaptosomes. Male rat brains were collected in ice-cold sucrose (0.32M) and homogenized, and by differential centrifugation we prepared P2 pellet. The pellet was then incubated with 3H-met-enkephalin, the reaction terminated by dilution, and the reaction mixture filtered under vacuum. (1) Lysing the synaptosomes in ice cold water before or after incubation with met-enkephalin separates out the synaptic vesicles. The post-incubation lysis showed a market amount of radioactivity in the supernatant which contained the vesicles. The vesicles may thus be the sites of accumulation of met-enkephalin. Pre-incubation lysis produced markedly less accumulation of radioactivity. (2) Ca++ at various concentrations was found to be an activator of met-enkephalin uptake. (3) The rate of accumulation of met-enkephalin was found to be temperature sensitive; 37 degrees greater than 25 degrees greater than 0 degrees. (4) The degree of uptake varied with different concentrations of met-enkephalin and with time. That it is the met-enkephalin taken up and not the degraded fraction was confirmed by RIA of the material extracted from the synaptosomes. The evidence provided here suggests that there is an uptake system for met-enkephalin.
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PMID:Synaptic mechanism of methionine-enkephalin uptake. 716 47

Systemically administered beta-endorphin was tested in rats for its ability to modify the hypothermia and hypermotility induced by d-amphetamine. Colonic temperature and motor activity were measured in a cold (4 degrees C) ambient temperature in animals given IP injections of beta-endorphin (0.1, 1.0 or 3.0 mg/kg), naloxone (10 mg/kg), or morphine (30 mg/kg). The same measurements were taken in animals given beta-endorphin (1.0 mg/kg) in combination with naloxone or saline pretreatment and d-amphetamine (15 mg/kg) or saline post-treatment. Morphine alone had a biphasic effect on thermoregulation, but did not affect d-amphetamine-induced hypothermia. Activity scores were decreased by morphine, in both d-amphetamine and saline treated animals. The thermal response of rats to beta-endorphin alone was variable, depending on dosage, but all 3 dosages partially blocked the hypothermic effect of d-amphetamine. Naloxone blocked the thermal effects of both beta-endorphin and d-amphetamine. Motor activity tended to be decreased by naloxone, regardless of amphetamine treatment, but beta-endorphin tended to increase activity in amphetamine-treated animals and reduce it in saline-treated controls. In their action on both thermoregulation and activity, naloxone and beta-endorphin appeared to interact independently with d-amphetamine, often producing effects in the same direction, but in combination, they tended to be mutually inhibitory.
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PMID:D-Amphetamine-induced hypothermia and hypermotility in rats: changes after systemic administration of beta-endorphin. 724 18

Early evidence has indicated the presence and involvement of specific neural systems which can inhibit the responses to painful stimuli. More recently, further advances suggest that the opiate system may interact with other systems to modulate the analgesia produced by the opiates or various stressors. Since corticosteroids were found to be elevated under the conditions of different stress-induced analgesia (SIA), there may be interactions between the pain-inhibiting systems and the corticosteroids. Recently it was reported that acute stress or long-term adrenalectomy can result in release of beta-endorphin (beta E) and ACTH from the pituitary gland, which can be blocked by dexamethasone. In our early studies we have shown partial antagonism of the SIA by dexamethasone and complete antagonism after naloxone. In this report it was found that chronic treatment of the rats with 0.02% metyrapone in drinking water for 8 weeks resulted in minor hyperalgesia. The chronic pretreatment with metyrapone resulted in a significant potentiation of the analgesia induced via the cold swim stress model, which was reversed by 1 mg/kg (IP) naloxone. Also, hyperalgesia was noted 18 days after the bilateral adrenalectomy of the rats as measured in our laboratory by the hot plate method and as reported by Heybach and Vernikos-Danellis in 1978. These results suggest that the corticosteroid modulation (pituitary-adrenal axis) may have a role in regulating the SIA, and this may implicate the interactions of the corticosteroids with pain-inhibiting systems.
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PMID:Corticosteroid modulation and stress-induced analgesia in rats. 730 Oct 53

Three groups of chick embryos were subjected to periodic cold exposures at the 1st (I), 2nd (II) and 3rd (III) weeks of incubation. Within the first month after hatching, glucocorticoid content of the blood plasma was measured in chicks. The reaction of the adrenals to corticotropin was checked in 2-month chicks. The activity of the adrenals was higher in the chicks from group III: they exhibited higher glucocorticoid concentration at the first week after hatching and later had more intensive reaction to ACTH. The rate of the adrenal reactions was also higher in group II. It was demonstrated that during the imprinting of thermal influences, glucocorticoid concentration in the blood plasma rapidly increases. The relation of the imprinting to ontogenetic re-arrangements in the endocrine system is discussed.
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PMID:[Imprinting of temperature effects in the embryogenesis of the hypothalamo-hypophyseal-adrenal system of domestic hens]. 746 12

We demonstrated the presence of opioid receptors in the porcine ovary using [3H]naloxone. We also examined the change in the number of opioid receptors during follicular maturation. In addition, we found specific binding of [3H]naloxone in the porcine ovary using naloxone, beta-endorphin, methionine-enkephalin and dynorphin. The binding of [3H]naloxone to porcine granulosa cells and the 2000-g subcellular fraction of corpora lutea was examined to demonstrate the presence of specific [3H]naloxone binding in the porcine ovary. Binding of [3H]naloxone to porcine granulosa cells was displaced by cold naloxone and beta-endorphin but not by dynorphin and methionine-enkephalin. A similar phenomenon was also demonstrated in the 2000 g subcellular fraction of porcine corpora lutea. However, Scatchard analyses revealed a single class of high-affinity (Kd = 28.5 x 10(-9) mol/l) and low-capacity binding sites (Bmax = 30.5 fmol/5 x 10(6) cells) in porcine granulosa cells. Similar binding parameters were obtained in the 2000-g subcellular fraction of porcine luteal tissue (Kd = 28.3 x 10(-9) mol/l, Bmax = 59.3 nmol/kg protein). [3H]Naloxone binding sites in the porcine ovary showed binding characteristics similar to those of opioid receptors in other organs like brain, uterus and placenta. Furthermore, we demonstrated that the specific binding sites of [3H]naloxone in porcine granulosa cells decreased during follicular maturation. Opioid receptors have been detected in the uterus, placenta and Sertoli cell cultures in some species. However, there is no detailed study on opioid receptors in granulosa cells and luteal tissues in any species. Our data suggest a relationship between folliculogenesis and ovarian opioid peptides.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[3H]naloxone binding sites in porcine ovarian follicles and corpora lutea during the ovarian cycle. 774 6

The availability of the most selective, high-affinity, natural opioid agonists for mu-receptors (dermorphin-DM) and delta-receptors (deltorphin-DT) has provided the possibility for in vivo studying of the role of acute and chronic activation of mu- and delta-opioid receptors on the functional activity of the hypothalamus-pituitary-adrenocortical (HPA) axis, both in basal conditions and in response to an acute stress in adult male rats. Plasma corticosterone (CS) and beta-endorphin-like-immunoreactivity (beta-EP-LI) levels were measured by specific radioimmunoassays before and after 5 and 30 minutes from the exposure to cold (3 +/- 0.5 C) water and forcing them to swim for 10 minutes (acute cold swimming stress). Acute administration of DM, the specific mu-receptor agonist, enhanced basal and stress induced plasma levels of CS and beta-EP-LI. These effects were antagonized by pretreatment with naloxone, specific mu-opioid receptor antagonist, but not by naltrindole, a delta-opioid receptor antagonist. Long-term administration of DM did not alter resting plasma levels of CS and beta-EP-LI, but significantly reduced stress-induced increase of these hormones. Both the acute and chronic administration of the DT, highly selective delta-opioid receptors agonist, failed to modify resting and stress induced hormone levels. Our present data show that DM throughout mu-opioid receptors, but not DT, modulates the response of HPA axis to acute stress in rats, increasing or decreasing the release of CS and beta-EP-LI when acutely or chronically administered, respectively.
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PMID:Involvement of mu-opioid receptors in the modulation of pituitary-adrenal axis in normal and stressed rats. 775 79

The effect of the palatability of a meal was tested on the post-prandial release of several gut hormones or neuropeptides which are known to have an effect on intake and satiety. Hormonal response was determined in plasma during the 3 h after a highly palatable and energy-rich meal or after the same meal served cold in a poorly acceptable form, as well as while fasting. The early post-prandial pancreatic polypeptide and neurotensin response was significantly higher after the highly palatable meal than after the cold one. Later responses differed only for pancreatic polypeptide. No difference was observed in cholecystokinin and neuropeptide Y levels. Post-prandial levels of beta-endorphin were elevated only after the cold meal and were associated with an elevated response of ACTH. We suggest that beta-endorphin might be secreted in response to an aversion towards the non-palatable cold meal. This could, subsequently, inhibit the cephalic phase of pancreatic polypeptide response and the early post-prandial response of neurotensin by a central anticholinergic effect. This study evidences an effect of palatability on the modulation of the digestive hormonal response after a meal.
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PMID:Palatability of a meal influences release of beta-endorphin, and of potential regulators of food intake in healthy human subjects. 797 41


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