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)

(D-ala2)-methionine-enkephalinamide (DAME) was injected into the third cerebral ventricle of unrestrained cats. At ambient temperature (Ta) = 22 degrees C, 3.1-50 micrograms caused dose-related hyperthermias. As dosage was increased, the hyperthermias diminished and in some cats hypothermia developed. Hyperthermia was not due to pyrogenic contamination or prostaglandin synthesis since it was not altered by pretreatment with a large IV dose of indomethacin. However, pretreatment with naloxone did cause a dose-related reduction in the hyperthermia. A low dose of DAME (12.5 micrograms) also caused hyperthermia at Ta = 4 and 32 degrees C, indicative of an increase in the level about which body temperature was regulated. On the other hand, a dose of 200 micrograms, which caused hyperthermia Ta = 22 and 32 degrees C, usually caused hypothermia at Ta = 4 degrees C, perhaps due to impairment of thermoregulatory control mechanisms. The response to DAME in the cold was reduced by naloxone pretreatment or reversed by subsequent injection of naloxone. Differences in hyperthermic patterns over a range of TaS and the lack of hypothermogenic action of morphine indicate that DAME alters thermoregulation in the cat by acting on morphine-insensitive, but naloxone-sensitive receptors. Central injection of beta-endorphin (5-50 micrograms) caused a dose-related hyperthermia. (Des-tyr1)-leucine-enkephalin (10-250 micrograms) was weakly hyperthermogenic, and kyotorphin (500 micrograms) did not consistently alter body temperature.
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PMID:Thermoregulatory effects of (D-ala2)-methionine-enkephalinamide in the cat. Evidence for multiple naloxone-sensitive opioid receptors. 625 Jun 78

Phosphatidylcholine (PC) synthesis in cultured fetal rabbit lung cells was studied after exposure to various pituitary peptides. Because of reports of an association between lung maturation and prolactin, 2 different preparations of ovine prolactin were studied in concentrations ranging from 0.1 to 10.0 microgram/ml. Increased saturated phosphatidylcholine (SPC) synthesis without an increase in synthesis of total PC, and increased SPC/PC, was observed after exposure to Sigma prolactin. NIH prolactin in the same concentrations had no effect on synthesis of either PC or SPC. Adrenocorticotropic hormone, luteinizing hormone and thyroid stimulating hormone increased synthesis of both PC and SPC, but none increased the SPC/PC ratio. A cold ethanol extraction of Sigma prolactin yielded fractions with no demonstrable biologic activity, and other initial attempts to characterize the active factor in the Sigma prolactin samples were unsuccessful. We concluded that prolactin per se has no direct effect on PC or SPC synthesis in the lung, but that certain other pituitary peptides have a direct effect on lung synthesis of PC and SPC.
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PMID:Pituitary oligopeptide regulation of phosphatidylcholine synthesis by fetal rabbit lung cells: lack of effect with prolactin. 626 36

ACTH (1--24) and alpha-melanotropin (alpha-MSH), peptides previously shown to influence body temperature when administered centrally and to occur naturally in brain regions important to temperature control, were injected intracerebroventricularly (ICV) in rabbits. The peptides in doses of 1.25, 2.5 and 5.0 micrograms produced dose-related hypothermias in a 23 degrees C environment, and greater decreases in body temperature when the experiments were repeated in the cold (10 degrees C), but the largest dose had no effect on temperature in the heat (30 degrees C). These results indicate that the peptides do not reduce the central set-point of temperature control. Rather, they appear to selectively inhibit heat conservation and production responses. Five microgram of ACTH reversed vasoconstriction and inhibited rises in temperature caused by leukocytic pyrogen (LP) given IV and ICV. The same dose of alpha-MSH also reduced fever produced by IV and ICV LP, but the reduction was not as great as after ACTH. Both peptides (5 micrograms) also reduced temperature rises and vasoconstriction caused by ICV PGE2. ACTH reduced d-amphetamine-induced hyperthermia without altering vasoconstriction which suggests that this peptide can reduce temperature rises by inhibiting heat production alone. One of the most important findings was that the peptides are antipyretic in that they reduce fever at doses (0.25 microgram, ICV) that do not affect normal temperature. The powerful effects of these peptides on resting body temperature, hyperthermia and fever, together with their presence in brain tissue important to temperature control, suggest that the endogenous central peptides participate in thermoregulation, perhaps by limiting fever and influencing normal temperature.
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PMID:Hypothermic and antipyretic effects of centrally administered ACTH (1--24) and alpha-melanotropin. 627 Jun 34

During development of the calcitonin binding assay using rat brain particulate fraction, it was noticed that 125l-salmon calcitonin-l (125-SCT) was partly absorbed by the polypropylene tube surface in an irreversible manner. Absorption was partially prevented by cold SCT and complete prevention was achieved by bacitracin. Triton X-100, Brij 36T, and some Zwittergents in such concentration ranges which appeared not to disrupt the 125l-SCT binding ability of brain tissue. The brain fraction itself exhibited a similar preventive effect. The anti-absorbing effect of Brij 36T was also observed in an opiate receptor binding assay for beta-endorphin. These results led us to recommend that the binding assay for these peptides should be done only in the presence of an appropriate anti-absorbant.
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PMID:Absorption loss of peptides to the plastic tube in radioreceptor assay of calcitonin and beta-endorphin: protection by detergents. 628 68

Endorphin and ACTH-like materials levels in rat plasma and pituitary were measured by radioimmunoassay under baseline and cold stress conditions. Cold stress significantly increased plasma beta-endorphin and ACTH immunoreactivity. A rise in these two peptides was also found in the neurointermediate lobe of the pituitary, while in the anterior lobe their levels were unaffected. These findings suggest that the rise of beta-endorphin and ACTH content in the neurointermediate lobe occurs as a compensatory biosynthetic mechanism for the peptides released from the adenohypophysis.
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PMID:Cold stress in the rat induces parallel changes in plasma and pituitary levels of endorphin and ACTH. 629 39

Neurotensin (NT) and bombesin, which are heterogeneously distributed in both brain and gastrointestinal tissue of several mammalian species, inhibit the formation of stress-induced gastric ulcers in rats. Many other endogeneous neuropeptides have also been reported to be present in brain and gastrointestinal tissue. The present study was conducted to evaluate the effect of some of these peptides on the development of cold-restraint stress (CRS)-induced gastric ulcers in rats. In addition, the effect of thyrotropin-releasing hormone (TRH), which antagonizes many of the CNS effects of NT, was investigated to determine whether this tripeptide antagonizes the cytoprotective effect of NT in this CRS model. All peptides were initially administered intracisternally (ic) in doses equimolar to 30 micrograms NT. As previously reported, NT (30 micrograms, ic) completely prevented the development of gastric ulcers in rats exposed to three hours of CRS. Bombesin, beta-endorphin, substance P, and somatostatin also exhibited cytoprotective activity. Several other peptides studied in the CRS model exerted no significant effects on the development of gastric ulcers; these included cholecystokinin octapeptide, gastrin, leu-enkephalin, met-enkephalin, and bradykinin. Two peptides, vasoactive intestinal polypeptide and TRH, significantly increased the severity of gastric ulcerations. The cytoprotective effect of NT was dose dependent. In contrast, lower doses of beta-endorphin, substance P, and somatostatin were cytoprotective whereas higher doses were not. Finally, concomitant ic injections of TRH antagonized the cytoprotective effects of NT and bombesin, but not that of beta-endorphin. The present results suggest that certain brain peptides may participate in modulating the gastric mucosal barrier, thereby increasing or decreasing its vulnerability to stress-induced lesions.
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PMID:The effect of centrally administered neuropeptides on the development of stress-induced gastric ulcers in rats. 630 95

The objectives of this study were threefold. First, we investigated the effects of acute stressful stimuli on gastroduodenal feeding activity after a physiologic meal. Second, we explored the possible role of humoral mediators of these effects by measuring concurrently plasma levels of beta-endorphin, catecholamines, and several gut peptides. Third, we wished to determine whether or not the gut responded selectively to different types of central stimuli. Thus, in 12 healthy volunteers we studied the effects of vertigo and cold pain on the gastrointestinal motor response to a solid meal. Pressure activity was recorded by a low-compliance perfusion system. Plasma concentrations of beta-endorphin and gut peptides were measured by radioimmunoassay, whereas catecholamine levels were measured by high-pressure liquid chromatography. Blood pressure, pulse rate, and skin conductance were also monitored. Labyrinthine vertigo (by otic stimulation with 10 degrees C water; control, 37 degrees C water) and cold pain (immersing hand in 4 degrees C water; control, 37 degrees C water) were simultaneously induced after the meal in each subject according to a 2 X 2 factorial experimental design. Cold pain and labyrinthine stimulation alone or in combination significantly reduced the antral phasic pressure response to solids while elevating plasma levels of beta-endorphin and norepinephrine. These effects occurred within the first 20 min poststimulus and were associated with changes in blood pressure, pulse rate, and skin conductance. Further, in 2 of 6 individuals in whom vertigo was induced by labyrinthine stimulation, a phase 3-like burst of motor activity appeared in the duodenum and migrated aborally. We conclude that centrally acting external stimuli may severely disrupt antral feeding activity. Furthermore, concurrent elevations in plasma levels of beta-endorphin and norepinephrine raise the possibility that these substances may be involved as mediators of the central effects on the gut.
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PMID:Stress-induced gastroduodenal motor disturbances in humans: possible humoral mechanisms. 630 93

In the cat naloxone has little, if any, effect on temperature under usual laboratory conditions and does not reduce febrile responses to leukocytic pyrogen. Hence, endogenous opioid peptides that are antagonized by naloxone are not essential for induction of fever or for maintenance of normal temperature in the absence of appreciable thermal stress. The purpose of this study was to assess the contribution of such endogenous opioids to thermoregulation in cats exposed to more severe thermal and non-thermal stresses. Changes in temperature of unanesthetized cats were determined after third cerebral ventricular injections of large doses (100, 250 micrograms) of naloxone or saline vehicle. Naloxone had no appreciable effect on the temperature of cats acutely exposed to hot (34 degrees C) or cold (4 degrees C) environments, either before or after tolerance to morphine had been induced by progressively greater daily or twice-daily intraventricular doses of 10-70 micrograms morphine sulfate. Naloxone also did not significantly affect the temperature of cats subjected to neck-restraint or forced to stand on a small platform if they were to avoid contact with ice water. These results provide no indication that an endogenous opioid peptide, such as beta-endorphin, that is antagonized by naloxone contributes appreciably to thermoregulation in cats. They do not rule out the possibility that endogenous opioids, such as Met-enkephalin, that are not readily antagonized by naloxone are important for normal thermoregulation.
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PMID:Evidence against involvement of beta-endorphin in thermoregulation in the cat. 630 83

In previous experiments small doses of the opiate morphine produced greater hyperthermia in aged than in younger sub-human primates. To test whether this augmented response is due to enhanced sensitivity of CNS opioid receptors with age, beta-endorphin (0.625-5 micrograms), an endogenous opioid peptide, was injected into the lateral cerebral ventricle (ICV) of young (less than 9 years) and aged (greater than 9 years) squirrel monkeys. Significantly greater hyperthermias developed in the older primates after each dose. In the aged monkeys, all but the smallest dose increased core temperature about 1.5 degrees C within 1 hr after injection. Mean rectal temperature in the younger animals rose 0.5-0.7 degrees after all but the largest dose (1-1.5 degrees C rise). Both groups maintained an elevated body temperature after central beta-endorphin throughout the 5 hr recording period. 1.25 micrograms beta-endorphin given ICV in a hot environment (30 degrees C) caused greater hyperthermia in older animals. This dose given in the cold (18 degrees C) caused large changes in temperature of the aged monkeys, either hyperthermia or marked decreases, whereas the young primates developed only moderate rises in body temperature. The same dose of morphine sulfate (1.25 micrograms) ICV produced similar changes in core temperature in the two age groups in each ambient temperature. These results indicate that: (1) stimulation of CNS opioid receptors influences thermoregulation and (2) aging increases responsiveness to such stimulation.
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PMID:Beta-endorphin: effect on thermoregulation in aged monkeys. 632 33

9 mormally cycling women and 7 other women employing oral contraceptives (OCs) were tested during 5 phases (menstrual, follicular, ovulatory, luteal, and premenstrual) of their menstrual cycle. An anxiety inventory was administered and pain detection and pain thresholds in response to electric shock and the cold pressor task were determined. Venipunctures were also performed and the plasma of normally menstruating women later assayed for beta-endorphin. Analyses revealed that the variance but the not mean levels in peripheral beta-endorphin levels differed significantly (p0.01) across the menstrual cycle with the greatest amount of variance found during the ovulatory phase and the least during the luteal. The high variance during the period around ovulation was due to several subjects having extremely elevated beta-endorphin levels; this may have resulted from the occurrence of ovulation. Furthermore, a significant positive correlation between anxiety levels and beta-endorphin levels was found only during the menstrual phase. The absence of findings concerning cyclic variation in pain thresholds is contrary to earlier reports and indicates that such a phenomenon may be dependent on the paradigm employed.
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PMID:Plasma beta-endorphin, pain thresholds and anxiety levels across the human menstrual cycle. 632 71


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