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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently, our laboratory has reported that central administration of beta-endorphin to rat pups decreases hepatic and renal ornithine decarboxylase activity, a sensitive biochemical index of tissue metabolic activity. Since these organs are the major sites of insulin catabolism, it seemed possible that the plasma levels of this hormone could be altered by changes in central nervous system (CNS) beta-endorphin levels. In the current study we tested this hypothesis by administering beta-endorphin to rat pups intracisternally (ic), followed by insulin sc, and then analyzing for plasma levels of insulin and glucose at various times after the second injection. We found that the apparent biological half-life of administered insulin markedly increased in 6-day-old rats pretreated with beta-endorphin ic. Similarly, this neuropeptide prolonged the half-life of endogenous insulin, as indicated by a small but significant increase in the plasma levels of this hormone in animals given only beta-endorphin. As expected, hypoglycemia in rats injected with beta-endorphin and insulin was more pronounced than in animals given insulin alone. Naloxone administered ic reversed both actions of beta-endorphin, indicating the involvement of opioid receptors in the response. beta-Endorphin also altered insulin and glucose plasma levels in 2-, 10-, and 18-day-old rats, but there were no effects in 30-day-old animals at any of the doses used in these studies. Peripheral administration of beta-endorphin had no effect, indicating that CNS beta-endorphin's influences on insulin and glucose metabolism occur through brain-based mechanisms. The results from these studies suggest that CNS beta-endorphin may be an important modulator of insulin and glucose metabolism in preweanling rats. In as much as insulin is a major regulator of somatic growth, our findings further suggest that CNS beta-endorphin may have a major role in the control of growth during early postnatal development by influencing insulin homeostasis.
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PMID:Regulation of insulin and glucose plasma levels by central nervous system beta-endorphin in preweanling rats. 252 2

In rats beta-endorphin antiserum systemic injection decreased during 1-2 days the threshold of tail-shock and latency of tail-flick tests, and during subsequent 85 days increased the threshold of tail shock, but not changed the latency of tail-flick tests. Naloxone injection blocked the increasing of thresholds, but not changed the latency of tail tests. It is suggested that antiserum evokes the first inhibition and the second selective activation of endogenous antinociceptive opioid system with affinity to electric nociception.
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PMID:[The biphasic selective effect of an antiserum to beta-endorphin on pain sensitivity in rats]. 252 29

Measurements were made of the effects of intracerebroventricular treatment with beta-endorphin (BE; 100 ng) on the arginine-8-vasopressin (AVP) and oxytocin contents of rat hypothalamic and limbic brain areas (hippocampus, amygdala and septum). The hormone concentrations were determined by radioimmunoassay. The administration of BE resulted in a significant reduction of the AVP level in the amygdala in a naloxone-reversible manner. Naloxone (Nal) administered subcutaneously significantly increased the AVP content in the septum. The results revealed that BE and Nal had regionally specific effects on the activity of the vasopressinergic system but not on that of the oxytocinergic system in the brain.
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PMID:The effects of beta-endorphin on arginine-8-vasopressin and oxytocin levels in rat brain areas. 252 2

Effects of yohimbine, methysergide and naloxone given intrathecally (i.t.) and naloxone given intracerebroventricularly (i.c.v.) on inhibition of the tail-flick and hot-plate response induced by beta-endorphin and morphine given i.c.v. were studied in male ICR mice. Yohimbine (1.5 and 15 micrograms) and methysergide (1.5 and 15 micrograms) injected i.t. antagonized inhibition of the tail-flick response induced by morphine but not beta-endorphin administered i.c.v. On the other hand, naloxone (20 ng) injected i.t. antagonized inhibition of the tail-flick response induced by i.c.v. administered beta-endorphin but not morphine. Yohimbine and methysergide given i.t. did not antagonize inhibition of the hot-plate response induced by morphine nor did naloxone given i.t. antagonized i.c.v. beta-endorphin-induced inhibition of the hot-plate response. Naloxone given i.c.v. was more effective in antagonizing morphine-induced inhibition of the tail-flick and hot-plate response than inhibition induced by beta-endorphin given i.c.v. Naloxone at doses (0.1 and 1 microgram) which effectively reversed inhibition of the tail-flick response to i.c.v. morphine was not effective in reversing the i.c.v. beta-endorphin-induced inhibition of the tail-flick response. Our results indicate that beta-endorphin and morphine produce analgesia by stimulating separate types of opioid receptors, epsilon- for for beta-endorphin and mu- for morphine, and activate separate descending pain modulatory control systems. The supraspinal epsilon system stimulated by beta-endorphin is mediated by activation of spinal opioid receptors whereas the supraspinal mu system stimulated by morphine is mediated by activation of spinal alpha 2-adrenoceptors and serotonin receptors for the production of analgesia.
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PMID:Differential mechanisms mediating beta-endorphin- and morphine-induced analgesia in mice. 253 Oct 93

In a previous study in unanesthetized goats, we demonstrated that cerebrospinal fluid levels of beta-endorphin were significantly elevated after 2.5 h of inspiratory flow-resistive loading. Naloxone (NLX) (0.1 mg/kg) administration partially and transiently reversed the tidal volume depression seen during loading. In the current study, we tested the hypothesis that endogenous opioid elaboration results in depression of respiratory output to the diaphragm. In six studies of five unanesthetized goats, tidal volume (VT), transdiaphragmatic pressure (Pdi), diaphragmatic electromyogram (EMGdi), and arterial blood gases were monitored. A continuous NLX (0.1 mg/kg) or saline (SAL) infusion was begun 5 min before an inspiratory flow-resistive load of 120 cmH2O.l-1.s was imposed. Our data show that the depression of VT induced by the load was prevented by NLX as early as 15 min and persisted for 2 h. At 2 h, Pdi was still 294 +/- 45% of the base-line value compared with 217 +/- 35% during SAL. There was no difference in EMGdi between the groups at any time. However, the augmentation of Pdi was associated with a greater increase in end-expiratory gastric pressure in the NLX group. We conclude that the reduction in VT and Pdi associated with endogenous opioid elaboration is not mediated by a decrease in neural output to the diaphragm, but it appears to be the result of a decrease in respiratory output to the abdominal muscles.
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PMID:Naloxone alters the early response to an inspiratory flow-resistive load. 253 92

Intravenous injection of beta-endorphin antiserum lowered the threshold of the tail-shock reaction to nociceptive electrocutaneous stimulation in rats in the first 1-2 days and raised it in the following 2-3 months. Naloxone injection reversed the analgesic effect of antiserum to beta-endorphin. Administration of normal serum did not change the threshold of the nociceptive reaction and naloxone failed to alter its effect. It is suggested that the secondary protracted effect of antiserum to beta-endorphin is a result of activation of the endogenous opioid system as a rebound-effect to diminished liberation of beta-endorphin in the first phase of the action of its antiserum.
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PMID:[The prolonged analgesic effect of an antiserum to beta-endorphin in rats]. 253 46

The role of the neuropeptide beta-endorphin on interleukin 1 (IL-1) production by murine bone marrow-derived macrophages was assessed. Beta-endorphin by itself did not induce IL-1 generation. However, over a wide range of concentrations (10(-6)-10(-14) M) beta-endorphin potentiated lipopolysaccharide (LPS)- or silica-induced production of intracellular and extracellular IL-1. This enhancement by beta-endorphin was most evident when using suboptimal doses of LPS. Naloxone, a competitive inhibitor of beta-endorphin opioid receptor interactions, abrogated the enhancing effects of beta-endorphin on LPS-induced IL-1 production. Furthermore, LPS-induced IL-1 production by macrophages (in the absence of added beta-endorphin) was also partially inhibited following treatment with naloxone, suggesting that opioids derived from activated macrophages may also modulate IL-1 generation and secretion. Thus, beta-endorphin-opioid receptor interactions result in enhanced production of immunomodulators such as IL-1.
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PMID:Beta-endorphin regulates interleukin 1 production and release by murine bone marrow macrophages. 253 39

Experimental studies in animal models suggest that the endorphin system may be implicated in the pathogenetic mechanism of cerebral ischemic lesions. Naloxone has been shown to possess a beneficial effect on the neurologic deficit associated with cerebral ischemia in animal experiments, probably because of its endorphin antagonist properties. By contrast, the results of clinical trials are contradictory. Moreover, the true significance of high plasma levels of beta-endorphin in patients with acute focal cerebral infarct (AFCI) has not yet been elucidated. We have evaluated 23 patients with established AFCI, in whom plasma levels of beta-endorphin and corticotropin (ACTH) were simultaneously measured during the first 48 hours after the onset of the disease. The results were compared with those from a control group. In a subgroup of 9 cases new measurements were made after 7 days. In the patients with AFCI, significantly lower levels of beta-endorphin and ACTH than in the control group were found. One week later, a moderate nonsignificant increase in the plasma level of beta-endorphin was found. The localization and estimated size of the infarct area were not relevant. Probably, the plasma levels of beta-endorphin will need to be considered before naloxone therapy is indicated, and only if it is confirmed that the plasma levels of beta-endorphin reflect changes at the cerebral level, as the pathophysiological role of these opioids in AFCI has not yet been established.
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PMID:[Beta-endorphin in acute focal cerebral infarct]. 255 75

Endogenous opioid regulation of blood pressure is altered during stress in young adults at risk for hypertension. We studied the effects of the opioid antagonist naloxone on the secretion of corticotropin and beta-endorphin during psychological stress in young adults with mildly elevated casual arterial pressures. Naloxone-induced secretion of both corticotropin and beta-endorphin was significantly diminished in persons at enhanced risk for hypertension compared with the low blood pressure control group. Results suggest that opioidergic inhibition of anterior pituitary function is altered in hypertension development.
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PMID:Altered pituitary hormone response to naloxone in hypertension development. 255 3

The present study was undertaken in order to assess the influence of aging on the endogenous opioid control of gonadotropin and adrenocorticotropin/cortisol secretion in man. For this purpose, the capability of the opioid antagonist naloxone to increase circulating levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and cortisol was tested in male subjects of different ages. Thirty normal men were randomly chosen and divided into 3 groups by age: group I = 22-40 years (n = 10); group II = 41-59 years (n = 10); group III = 62-80 years (n = 10). Since the men of group III showed higher basal serum gonadotropin concentrations than the subjects of group I and group II, we selected from a large population a fourth group of elderly men with normal basal LH and FSH levels: group IV = 61-82 years (n = 7). All subjects were tested for 120 min during the intravenous administration of naloxone (4 mg given in an intravenous bolus at time 0, plus 10 mg infused for 2 h). Control tests with normal saline instead of naloxone were performed in all groups. All subjects had similar blood testosterone and cortisol levels, whereas LH and FSH concentrations were significantly higher in group III than in groups I, II and IV. Naloxone increased plasma cortisol concentrations by 50% in all groups. The cortisol secretory response followed a similar pattern regardless of age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Different effects of aging on the opioid mechanisms controlling gonadotropin and cortisol secretion in man. 256 Apr 54


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