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)

The plasma beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) response of men, eumenorrheic women, and amenorrheic women (n = 6) to 1 h of rest or to a bicycle ergometer test [20 min at 30% maximum O2 uptake (VO2max), 20 min at 60% VO2max, and at 90% VO2max to exhaustion] was studied in both normal (22 degrees C) and cold (5 degrees C) environments. beta-EP and beta-LPH was measured by radioimmunoassay in venous samples collected every 20 min during rest or after each exercise bout. Exhaustive exercise at ambient temperature (Ta) 22 degrees C induced significant increases in plasma beta-EP and beta-LPH in all subjects as did work at 60% VO2max in amenorrheic and eumenorrheic women. During work at Ta 5 degrees C, the relative increase in beta-EP and beta-LPH was suppressed in eumenorrheic women and completely prevented in amenorrheic women. Although significant lowering of beta-EP and beta-LPH was observed in men and eumenorrheic women during rest at 5 degrees C, amenorrheic women maintained precold exposure levels. These findings suggest that plasma beta-EP and beta-LPH may reflect a thermoregulatory response to heat load. There appears to be a sexual dimorphism in exercise- and cold-induced release of beta-EP and beta-LPH and amenorrhea may be accompanied by alterations in these responses.
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PMID:Exercise- and cold-induced changes in plasma beta-endorphin and beta-lipotropin in men and women. 295 62

The effect of beta-endorphin, met-enkephalin and leu-enkephalin on cold-stimulated TSH and prolactin secretion after infusion of the drugs into the 3rd ventricle or into the posterior hypothalamus (PH) was investigated in male rats. beta-endorphin (0.25 microgram/rat, but not 0.05, 0.5 and 1 microgram/rat) increased and met-enkephalin (20 and 100 micrograms/rat) decreased TSH secretion when infused into the 3rd ventricle. After bilateral infusion into the PH, beta-endorphin (0.25 microgram/side, but not 0.05 and 1 microgram/side) increased TSH secretion, but met-enkephalin (1 and 10 micrograms/side) induced no changes. beta-endorphin (0.05-1 microgram/rat) and met-enkephalin (100 micrograms/rat) both increased prolactin secretion when infused into the 3rd ventricle, but only a high dose of beta-endorphin (1 microgram/side) was effective after infusion into the PH. Leu-enkephalin had no effect on TSH or prolactin secretion at the hypothalamic level. These results favour the hypothesis that mu-receptors mediate the inhibitory effect and other types (possible epsilon-receptors) of opiate receptors mediate the stimulatory effect of opioid peptides on TSH secretion at periventricular sites. However, only stimulatory mu-receptors affect prolactin secretion at these sites. After infusion into the PH, the effect of a high dose of beta-endorphin on prolactin secretion may also be mediated through periventricular sites, but its effect on TSH secretion is evidently mediated through opiate receptors in the PH.
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PMID:Opioid peptides in the regulation of TSH and prolactin secretion in the rat. 295 56

Age-related decreases occur in analgesic responses following morphine, 2-deoxy-D-glucose, inescapable foot shock and cold-water swims. Decreased affinity and concentration of opiate receptors and levels of endogenous opioids are also observed. The present study evaluated the dose-dependent (0.1, 0.5, 1.0, 5.0 micrograms, ICV) and time-dependent (15, 30, 45, 60 min) properties of beta-endorphin analgesia on the jump test across three age cohorts of rats (8, 18 and 30 months of age). The different age cohorts failed to display differences in the magnitude of beta-endorphin analgesia across doses and times, except for a transient (30 min) decrease in the 30-month group following the 0.5 microgram dose. This maintenance of beta-endorphin analgesia across age cohorts stands in marked contrast to the age-related decrements in morphine and opiate-sensitive environmental analgesia and occurs despite decreased levels of beta-endorphin. These data are discussed in terms of differential alterations in opiate receptor subpopulations, and represent the first instance of maintained opioid analgesia across cohorts.
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PMID:Maintenance of beta-endorphin analgesia across age cohorts. 295 82

We investigated cardiac noradrenalin (NA) levels during stress (from cold and from swimming) and after i.p. administration of beta-endorphin. Cardiac NA levels were significantly increased by endorphin, 1.25 mg X kg-1, and decreased by 10 mg X kg-1. Beta-endorphin, 10 mg X kg-1, and cimetidine, 20 mg X kg-1, decreased cardiac NA to control levels in stressed animals. Naloxone given to stressed animals treated either with beta-endorphin or cimetidine elevated NA to control concentrations, but failed to restore NA to the elevated levels induced by stress. These results suggest endorphin involvement in enhanced NA levels in stress and a possible role of H2-receptors in this involvement.
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PMID:Effect of beta-endorphin and cold stress on heart noradrenalin levels in rats. 295 26

Repeated immunization of rats with beta-endorphin-bovine albumin conjugate (75:7.5 g) mixed with Freund's adjuvant (1:1) induced a significant decrease in beta-endorphin content in the pituitary body and hypothalamus. The immunized rats showed suppressed antinociceptive reaction to morphine (5 mg/kg, i.p.) and in unavoidable foot shock. Cold swimming stress did not influence the pain reactions, as compared to the control group. The results indicate that mechanisms of different types of analgesia involve selective neurochemical systems.
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PMID:[Comparative analysis of the role of beta-endorphin systems in the mechanisms of different types of analgesia]. 296 Mar 87

This study was designed to characterize physiological events related to a single or repeated experimental anaphylactoid reactions (by Compound 48/80) in non-stressed or cold-restrained rats. Acute treatment with Compound 48/80 (1 mg/kg, i.p.) increases Beta-endorphin(ir) content in the neurointermediate lobe (NIL) of rat pituitary. Moreover, repeated treatment with Compound 48/80 showed tolerance effects. These animals, exposed to stressful conditions, exhibited a fully evident paw oedema following carrageenin oedema-test, whereas saline-pretreated rats, under the same experimental conditions, showed reduced local inflammation. Since Compound 48/80 produces characteristic, systemic, anaphylactoid reaction in the rat, with a very high degree of selectivity in its action, our results suggest that mast-cell histamine and Beta-endorphin from NIL pituitary are involved in the body's reactivity to stressful stimuli.
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PMID:Evidence of correlations between mast-cell histamine and beta-endorphin (ir) from NIL-pituitary in the homeostasis. 296 95

The role of mast cell histamine in body reactivity of rats under experimental stressful conditions was studied. Animals submitted to chronic anaphylactoid reactions (by injecting compound 48/80 at the dose of 1 mg/kg, i.p., twice daily, for five days), when exposed to cold-restraint stress, exhibited a fully evident inflammatory response in the carrageenin-oedema test, whereas saline-treated rats, under the same experimental conditions, showed reduced paw oedema. Interestingly, a single injection of compound 48/80 increased the pituitary content of Beta-endorphin(ir), but chronic administration failed to produce this effect suggesting that some adaptation of the organism to repeated anaphylactoid reactions may occur. These results support the hypothesis of correlations between pituitary Beta-endorphin and mast cell histamine in the reactivity of the organism to stressful stimuli.
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PMID:Correlations between histamine and opioid peptides on the modulation of inflammatory processes in rats exposed to stress. 296 76

Cold stress produced a significant reduction in the concentration of immunoreactive beta-endorphin (IR-BE) in the anterior pituitary of diabetic female rats. IR-BE levels in the anterior pituitary of non-diabetic female rats were not affected by exposure to the cold. The effects of cold stress on IR-BE levels in the neurointermediate lobe of the pituitary and the hypothalamus were attenuated in diabetic as compared to control animals. These data suggest that in female rats, eight weeks of diabetes produced alterations in the neuroendocrine mechanisms which modulate IR-BE levels in the pituitary and hypothalamus in response to cold stress.
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PMID:Eight weeks of streptozotocin-induced diabetes influences the effects of cold stress on immunoreactive beta-endorphin levels in female rats. 297 9

The role of corticotropin-releasing factor (CRF) in four model stresses (cold, ether, immobilization, and trauma) was examined in the guinea pig by using passive immunoneutralization with anti-CRF antiserum. Plasma corticotropin levels were measured at various times after exposure to stress, and groups treated with CRF antiserum were compared with those treated with normal rabbit serum. Of the four stresses tested, ether had the most pronounced effect on corticotropin secretion. Treatment with anti-CRF inhibited most of the ether-induced corticotropin secretory response, the difference between the normal serum- and the anti-CRF antiserum-treated groups being significant at 5 and 10 min (P less than 0.01). Corticotropin responses to cold stress in the two groups differed at the 0.05 level of significance at 10 and 20 min. After administration of trauma (leg fracture), a statistically significant difference (P less than 0.01) between the two groups also was evident, albeit only at 20 min. During immobilization, corticotropin levels differed significantly from control only in the normal serum-treated group but not in the anti-CRF-treated group. These findings show that CRF antiserum was effective in reducing corticotropin levels, indicating that CRF has an important role in mediating corticotropin response to stress. The fact that neutralization was incomplete might be due to an inability of the antiserum to sufficiently neutralize the endogenous CRF or, more likely, reflects the contribution of additional mediators, notably catecholamines and vasopressin, of corticotropin release upon stress.
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PMID:Evidence for a role of endogenous corticotropin-releasing factor in cold, ether, immobilization, and traumatic stress. 298 31

In each of two trials, plasma corticosterone (B) was measured in Large White turkey tom poults after the following treatments were applied: 1) .9% saline injected; 2) cold water immersion, and 3) adrenocorticotropic hormone (ACTH) injected (10 IU/kg body weight). Poults were treated at 3- to 4-day intervals from the day of hatching to 21 days of age. Plasma samples were obtained at 1, 2, 3, 4, and 6 hr posttreatment. In both trials, there was a depression in B levels within the first 3 hr following ACTH or cold water immersion treatment. Significant increases in plasma B levels of the cold water treatment occurred at 4 hr posttreatment in Trial 1 in 7-day-old poults and in Trial 2 in 21-day-old poults. A significant adrenal cortical response to ACTH injection was observed in 3- and 7-day-old poults at 6 hrs posttreatment in Trial 2. Plasma B concentrations were also measured in three groups of nontreated Large White tom poults on the day of hatching at a commercial hatchery. Plasma samples were obtained from poults in incubators at 1000 hr, immediately following commercial processing procedures at 1030 hr, and at poult placement at 1330 hr. Plasma B levels of poults sampled in the incubator and after processing were similar. However, B levels of poults sampled at placement were increased significantly above the other two groups.
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PMID:Adrenal cortical response of tom poults. 299 46


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