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-situ hybridization histochemistry was used to measure corticotrophin-releasing factor mRNA and proenkephalin A mRNA in the paraventricular nucleus (PVN), and pro-opiomelanocortin (POMC) mRNA in the anterior pituitary of the rat. Levels of message were determined at 1, 2, 4 and 8 h after exposure to a variety of physical and psychological stresses. Corticotrophin-releasing factor mRNA in the PVN and POMC mRNA in the anterior pituitary increased in response to i.p. hypertonic saline, restraint and swim stress but not to cold stress. Proenkephalin A mRNA was raised only in response to the physical stress of i.p. injection of hypertonic saline. These results suggest that different afferent pathways and hypothalamic neurotransmitters may be involved in mediating the hypothalamic response to different physical and psychological stresses.
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PMID:Responses of hypothalamic and pituitary mRNA to physical and psychological stress in the rat. 280 78

Neonatal rats show a period of diminished adrenocorticotropin responsiveness to stress during the first 2 weeks of life. To test whether beta-endorphin-like peptides (beta-EPLPs) follow the same pattern of hyporesponsiveness to stress during this period, we examined the ontogeny of the beta-EPLPs response to two different types of stressors (ether vapors and cold) during the early postnatal period. The content of beta-EPLPs was estimated in the serum, the pituitary gland and the hypothalamus prior to and 5 min following exposure to stressful stimuli. Furthermore, to determine the relationship between the responsiveness of beta-EPLPs to stress and that of the hypothalamic-pituitary-adrenal axis in the developing rat, the content of hypothalamic corticotropin-releasing factor (CRF) and serum corticosterone was estimated prior to and following stress. Results indicated that stress induced an increase in the serum corticosterone levels at all ages tested (days 1-22), however, the stress-induced elevations of serum corticosterone were significantly greater on days 1 and 22 than on days 3-14. Significant stress-induced elevations of serum immunoreactive beta-endorphin (ir-beta-EP) were observed on days 14 and 22 of life, while changes on days 1, 3, 8 and 10 were either nonexistent or not statistically significant. Gel filtration analysis revealed that the increases in serum ir-beta-EP following stress on days 14 and 22 resulted primarily from increases in the beta-lipotropin component with lesser increases in the beta-endorphin component. Pituitary content of beta-EPLPs was not affected by stress before day 10, but was markedly reduced in the 10- and 14-day-old rats, following stress. A similar, although not statistically significant decrease was observed in the pituitary content of beta-EPLPs of the 22-day-old rats after exposure to stress. Furthermore, exposure to cold stress in the 14-day-old rats induced more pronounced changes in the serum ir-beta-EP and corticosterone levels as well as in the pituitary ir-beta-EP content than it did with ether stress. Despite variations in serum corticosterone as well as serum and pituitary content of beta-EPLPs, no changes in the hypothalamic ir-beta-EP content were seen in rats after subjection to stress, while small, not statistically significant reductions in the hypothalamic CRF content were observed at 5 min after the onset of stress in the 14-and 22-day-old rats. Thus, during the first 2 weeks of life neonatal rats exhibit a reduced capacity to secrete beta-EPLPs in response to stress.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Ontogeny of the beta-endorphin response to stress in the rat: role of the pituitary and the hypothalamus. 281 72

Three trials were conducted to investigate plasma corticosterone (B) levels in Large White turkey hens in response to adrenocorticotropic hormone (ACTH) injections at different ages, doses, and routes of administration. In Trial 1, hens were subjected to one of the following treatments at 10, 15, and 20 wk of age: cold water immersion (5 C for 1 min), ACTH injection (10 IU/kg), or saline injection. The plasma B responses to ACTH and cold water immersion followed the same general pattern in all three age groups. Plasma B levels of hens in the ACTH treatment were depressed below control B levels until 6 h postinjection, when they became elevated. Plasma B levels of hens in the cold water treatment were either similar to or increased above those of controls by 2 h posttreatment and were depressed below control levels at .5 h posttreatment at 10 and 15 wk of age. In Trial 2, three dose levels of ACTH (1, 5, and 10 IU/kg) were injected either intramuscularly (IM) or intravenously (IV) in 10-wk-old hens. There was both a dose and route of administration effect. Of the IM-injected hens, only those in the 1-IU ACTH treatment group had significantly (P less than .05) increased plasma B levels and this occurred 4 h postinjection. However, plasma B levels of the 1 and 5-IU IV-ACTH treatment hens were significantly (P less than .05) elevated at .5 h postinjection. Plasma B of the 10-IU IM and IV-ACTH treatments were consistently, but not significantly, lower than controls through 4 h postinjection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma corticosterone response of turkeys to adrenocorticotropic hormone: age, dose, and route of administration effects. 282 52

Bilateral microinjections of the opiate antagonist naloxone (0.1, 1.0 and 10.0 micrograms) into the central nucleus of the amygdala (CEA) produced a significant potentiation of cold restraint-induced gastric pathology in rats. The opiate agonist, beta-endorphin (0.1, 1.0 and 10.0 micrograms), on the other hand, inhibited stress ulcer formation in a dose-related manner. Stress ulcer-attenuating effects were also seen with intra-CEA injections of the enkephalin analogs [D-Ala2,D-Leu5]enkephalin (10.0 micrograms) and [D-Ala2]Met-enkephalinamide (10.0 micrograms). Pretreatment of rats with naloxone (1.0 microgram) completely antagonized and even reversed the gastric cytoprotective effects of beta-endorphin (1.0 and 10.0 micrograms). The results indicate that the CEA is important in the gastric cytomodulatory effects of endogenous opiates during stressful experiences.
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PMID:Opiate mechanisms in the central amygdala and gastric stress pathology in rats. 283 14

The purpose of this study was to characterize the central metabolism/processing of beta-endorphin in wild, desert rodents and to study the effect of heat and cold acclimation on central metabolism/processing and beta-endorphin half-life. This report suggests that a shift occurs in the processing of beta-endorphin in desert rodents acclimated to heat and cold leading to an accumulation of gamma-type endorphins. The data support a significant difference in beta-endorphin half-life between the rodents and the laboratory white rat.
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PMID:Central metabolism of beta-endorphin in different species of temperature acclimated rodents. 287 40

The hyperphagia and obesity induced by ventromedial hypothalamic (VMH) electrolytic lesions in female rats were associated with a 70-94% decrease in the level of beta-endorphin (beta-E) in the hypothalamus and other regions of brain, but not in the pituitary. Dynorphin (Dyn) and methionine-enkephalin (ME) levels were also decreased. Rats with VMH lesions were less sensitive to the inhibitory effect of naloxone on their food-intake. Mice injected with gold thioglucose (GTG) also showed a decrease in the hypothalamic content of beta-E and Dyn and exhibited 30% less analgesia compared to control mice after cold swim stress.
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PMID:Effect of electrolytic and chemical ventromedial hypothalamic lesions on food intake, body weight, analgesia and the CNS opioid peptides in rats and mice. 289 79

Using a rat tail-flick analgesic assay that uses a cold water-ethylene glycol mixture (-10 degrees C) as the noxious stimulus, we have been able to demonstrate a dose-related, naloxone-reversible analgesic effect for dynorphin A (1-17), the proposed endogenous ligand for the kappa receptor. Male Sprague-Dawley rats were implanted surgically with cannulas in the right lateral ventricle at least 1 week before testing. Five microliters of either drug or saline, followed by a 3-microliter saline flush, were administered. Nociceptive threshold was measured as the latency for the rat to flick or remove its tail from the bath solution after immersion. Dynorphin produced a dose-related analgesia at doses of 1 to 50 micrograms i.c.v., reaching 100% maximum possible analgesia (compared to predrug base line) at the highest dose. We found similar dose-related analgesia when we tested the selective mu agonist [Try-D-Ala-Gly-NMe-Phe-Gly-ol] (0.01-1 microgram), the selective kappa receptor ligand U-50,488H (100-500 micrograms), the selective delta agonist [D-Pen2,5]-enkephalin (50-200 micrograms) and beta-endorphin (0.1-10 micrograms). Naloxone (1.0 mg/kg) was able to block the antinociceptive effect of all but the highest doses of dynorphin, which required 10.0 mg/kg of naloxone. When we compared the same dosages of dynorphin using hot water (55 degrees C) as the noxious stimulus, no antinociception was observed. Although we do not known the mechanisms responsible for the differences between the hot and cold water tests, it may be that the cold water tail-flick test, which is able to assess the antinociceptive activity of both opioid agonists and mixed agonist-antagonists, is a more sensitive measure of the type of analgesia mediated by kappa receptors.
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PMID:Antinociceptive action of intracerebroventricularly administered dynorphin and other opioid peptides in the rat. 290 Mar 24

In humans, plasma beta-endorphin levels rise during application of acute stressful stimuli (vertigo, cold pain, and transcutaneous electrical stimulation) that induce gut motor disturbances. Whereas it is possible that circulating beta-endorphin participates in the mediation of these central effects on gut motility, its role cannot be established solely on the basis of changes in plasma levels. Therefore, we designed the present study to investigate 1) the dose-related effects of intravenous synthetic human beta-endorphin and naloxone on gastrointestinal pressure activity in fed healthy individuals; and 2) the interactions of the opiate agonist and antagonist. Infusion of beta-endorphin increased pyloric phasic pressure activity (P less than 0.001) and induced intestinal bursts of rhythmic activity (P less than 0.05) which interrupted normal fed motility. These effects were dose related, with the pyloric dose-response profile being essentially linear. The effects in the proximal intestine were obtained with doses of beta-endorphin at 250 ng X kg-1 X min-1 or greater. In the antrum, there was an overall reduction in phasic pressure activity (P less than 0.02), which was predominantly an effect of the highest dose of beta-endorphin infused (2,500 ng X kg-1 X min-1). Naloxone by itself had no significant effect on fed upper gut motility. However, naloxone significantly inhibited the effect of the lower doses of beta-endorphin on the pylorus. In addition, naloxone significantly reduced the probability of beta-endorphin, triggering intestinal bursts of rhythmic activity. These data suggest that beta-endorphin may play a humoral role in the stimulation of fed pyloric contraction at physiological levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dose-related effects of synthetic human beta-endorphin and naloxone on fed gastrointestinal motility. 294 39

Concentrations of endogenous opioid peptides in the plasma are increased during exercise and these substances have been implicated in the pathogenesis of asthma induced by chloropropramide and alcohol in diabetic patients. This work was undertaken to determine whether exercise induced asthma might be mediated by endogenous opioids. Plasma beta endorphin, met-enkephalin, and adrenocorticotrophic hormone (ACTH) concentrations were measured in five asthmatic patients and five normal volunteers breathing cold air during exercise. In four of the patients the effect of an infusion of naloxone on FEV1 was also measured during exercise induced asthma. Exercise produced acute bronchoconstriction in all asthmatics, characterised by a fall in FEV1; whereas no change occurred in normal subjects. There was no difference in plasma met-enkephalin, beta endorphin, and ACTH concentration between the two groups. Infusion of naloxone neither prevented nor worsened exercise induced asthma. These data suggest that endogenous opioids probably do not play a part in the development of exercise induced asthma.
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PMID:Exercise induced asthma and endogenous opioids. 294 40

Growing evidence indicates that most patients with coronary artery disease frequently have episodes of painless myocardial ischemia. Previous studies from our institution show that the severity and duration of myocardial ischemia are necessary but not sufficient factors to explain the occurrence of anginal pain. The responses to a battery of painful stimuli were studied in 12 patients with predominantly painless (group A) and in 15 patients with predominantly painful (group B) ischemic episodes. The severity of myocardial ischemia as assessed by the measurement of ST-segment depression during exercise stress testing and during ambulatory electrocardiographic monitoring was comparable in the 2 groups. Patients in group A had a significantly higher threshold and tolerance for forearm ischemia (+32%, p less than 0.05; +120%, p less than 0.001), cold (+100%, p less than 0.05; +180%, p less than 0.01) and electrical skin stimulation (+145%, p less than 0.01; +109%, p less than 0.01), but the overlap between the 2 groups was often appreciable. In the 6 patients with the longest tolerance times for forearm ischemic pain (all in group A) and in the 5 having the shortest tolerance times (all in group B), plasma levels of beta endorphin, met-enkephalin, noradrenaline and adrenaline were similar during both the basal state and the induction of forearm ischemic pain. Thus, a generalized defective perception of painful stimuli plays an important role in many patients with predominantly painless myocardial ischemia. Other mechanisms, however, may also be important, particularly in patients whose threshold and tolerance values overlap with those of patients who have predominantly painful myocardial ischemia.
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PMID:Importance of generalized defective perception of painful stimuli as a cause of silent myocardial ischemia in chronic stable angina pectoris. 294 17


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