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 peptidergic, endogenous opioid system counteracts exogenous and endogenous stress factors. The system will be activated by stress, e.g., also in case of heart failure. The endogenous opioids endorphin, met-enkephalin, leu-enkephalin, dynorphin, casomorphin, and others split from precursor proteins (250-265 amino acids) by a specific proteolytic cleavage. In clinical and experimental heart failure the plasma levels of endorphin and lipotropin are changed as an evidence of the activated opioid system. In patients with chronic heart failure the plasma levels of endorphin and lipotropin are decreased, which is discussed as an exhaustion of the opioid system. In the case of experimentally induced right-heart failure in dogs the plasma levels of endorphin and lipotropin are increased. Morphine antagonists (naloxone hydrochloride) which penetrate into the cerebral system improve the disturbed hemodynamics in dogs with a right-heart failure. The improving effects results from central actions since opiate antagonists, which cannot penetrate the blood-brain-barrier (naloxone methobromide) have no effect. The actions of opioid peptides will be induced by inhibition of the depletion and the reabsorption of catecholamines in synaptic storages (isolated atria from guinea pig). In cultures from cardiac myocytes (chicken ventricle cells) enkephalins induced positive inotropic effects via receptor mediated mechanisms. The results showed modulating activities of endogenous opioids against the effect of activated sympathetic activity.
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PMID:[Role of endogenous opioids in heart failure]. 166 29

Morphine releases endogenous opioids into the circulation of dogs. To test the stereospecificity of this effect, as well as to determine whether morphine also releases endogenous opioids centrally, which might be involved in its antinociceptive action, the effects of (-)-morphine sulfate (10 mg/kg, sc) or (+)-morphine hydrobromide on antinociception in a dog tail-flick test, on semi-quantified morphine-induced signs of salivation, emesis, defecation and ataxia, and on the plasma and cerebrospinal fluid (CSF) levels of endogenous opioid peptides were studied. Plasma and CSF levels of immunoreactive beta-endorphin (i-BE), met-enkephalin (i-ME), leu-enkephalin (i-LE), and dynorphin (i-DY) were quantified by radioimmunoassay in octadecylsilyl-silica cartridge extracts. Immunoreactive morphine (i-M) levels were measured in unextracted samples. (-)-Morphine treatment significantly increased antinociception, morphine-induced signs, i-M levels in plasma and CSF, and i-BE, i-ME, and i-LE levels in plasma, but not CSF. Levels of i-DY remained constant in plasma and CSF. (+)-Morphine treatment did not alter any of these parameters, indicating that the effects of morphine on nociception, behavioral signs, and plasma endogenous opioids in dogs were stereoselective. It is concluded that morphine does not cause an increase in immunoreactive endogenous opioid peptides in the CSF at the time of its peak antinociceptive effect.
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PMID:Stereoselective effect of morphine on antinociception and endogenous opioid peptide levels in plasma but not cerebrospinal fluid of dogs. 167 91

The experiments examine the actions of morphine and opioid peptides on the responses evoked by electrical field stimulation or by acetylcholine (ACh) and substance P (SP) in guinea-pig bronchial strip chain. Electrical field stimulation evoked a biphasic contraction, consisting of a cholinergically mediated fast contraction followed by a non-cholinergically mediated slow contraction. Morphine and opioid peptides caused a concentration-dependent inhibition in the height of the non-cholinergic contraction. The order of inhibitory activity was BW443C greater than dynorphin greater than morphine greater than beta-endorphin greater than leucine-enkephalin greater than methionine-enkephalin. Cholinergically mediated contractions were less potently inhibited by these opioids. Submaximal contractions of bronchial muscle evoked by exogenous ACh (2 microM) or SP (0.2 microM) were not inhibited by morphine (100 microM) or opioid peptides (3-10 microM), rather, they were augmented. The results indicate that in guinea-pig isolated bronchial muscle, morphine and opioid peptides can selectively inhibit excitatory non-cholinergic neurotransmission via prejunctional opioid receptors.
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PMID:Morphine and opioid peptides selectively inhibit the non-cholinergically mediated neurogenic contraction of guinea-pig isolated bronchial muscle. 169 28

Morphine, leu-enkephalinamide, met-enkephalin, alpha-neoendorphin and its Arg8 1-8 fragment increase contractile vacuole output in the freshwater Amoeba proteus at 18 microM. Significant effects of leu-enkephalin and naloxone are obtained at 180 microM. All compounds have reached their maximal activity at 720 microM. Alpha-neoendorphin and leu-enkephalin are inactive in the presence of isotonic, non-penetration sucrose, hence these compounds increase plasma membrane permeability to water. Results from molecular modeling show a clear correlation of activity with amphiphilicity, charge distribution and general flexibility of molecules. We conclude that, like previously-studied vasopressin analogues and non-hormonal amphiphilic peptides, active opioids embed themselves into the Amoeba plasma membrane, disrupting the lipid bilayer and increasing its permeability. In our Amoeba system, naloxone, a general morphine-like inhibitor, blocks active opioids as well as a vasopressin analogue. Naloxone, being less active than other tested amphiphiles, acts as a membrane stabilizer, protecting the lipid bilayer against the disruption action of more active compounds.
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PMID:Direct membrane effects of morphine and endorphins on Amoeba proteus. 173 Nov 68

Dose-response curves of three receptor-selective opioids were established in a group of nonburned and a group of burned rats. Morphine (mu-agonist), biphalin (mu- and delta-agonist), and U50488H (kappa-agonist) were administered to each group, and analgesia was measured by tail flick latency testing. Each opioid had a significant increase in potency (i.e., a decrease in ED50 values) in the burned (15% body surface area) compared with the nonburned groups. Moderate doses of each drug (i.e., ED50 doses estimated from nonburned group data) in each case augmented stress-induced analgesia in the burned group. Analgesic doses failed to prevent a significant increase in plasma beta-endorphin and corticosterone after larger surface area (25%) burns. Regardless of receptor specificity, opioid analgesic potency is increased acutely after burn injuries.
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PMID:Enhanced potency of receptor-selective opioids after acute burn injury. 189 68

Morphine and the synthetic opioid met-enkephalin analog [D-Ala2, MePhe4, Met(0)5ol] enkephalin (FK 33-824) injected intraperitoneally to rats at doses of 5-20 and 0.5-2 mg/kg respectively showed a protective effect on gastric lesion induced by cold-restraint stress. This protective effect was abolished by pretreatment with indomethacin. This suggests a role for prostaglandins in the protection, induced by opioids of the gastric mucosa against the development of stress-induced ulcers.
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PMID:Effect of indomethacin on opioid-induced gastric protection in cold-restrained stress. 199 88

The effects of beta-endorphin, D-Ala2-NMePhe4-Gly-ol-enkephalin (DAMGO) and morphine microinjected into raphe obscurus nucleus (ROb) and gigantocellular reticular nucleus alpha (GiA) in inhibiting the tail-flick response were studied in pentobarbital anesthetized rats. beta-Endorphin (0.1-3 micrograms) microinjected into ROb inhibited the tail-flick response dose-dependently and produced 100% inhibition at high doses (greater than 3 micrograms). DAMGO [0.004-0.015 micrograms] injected into ROb, also dose-dependently, inhibited the tail-flick response but reached a plateau of 60 to 80% inhibition at high doses (greater than 0.015 micrograms). Morphine (10-60 micrograms) injected into ROb produced only a small inhibition (less than 20% inhibition) even at high doses (greater than 60 micrograms). The rank order of potency of these opioids on the tail-flick inhibition was DAMGO greater than beta-endorphin greater than morphine. Morphine (1-10 micrograms) and DAMGO (0.004-0.03 micrograms) microinjected into GiA produced dose-dependent inhibitions of the tail-flick response and high doses of these two mu agonists fully inhibited the tail-flick response. However, beta-endorphin (0.1-10 micrograms) injected into GiA produced a small but dose-dependent inhibition of the tail-flick response (less than 60% inhibition). The rank order of potency of these opioids on the tail-flick inhibition was DAMGO greater than beta-endorphin greater than morphine. The inhibition of the tail-flick response induced by beta-endorphin (2 micrograms) microinjected into ROb was blocked by the coadministration of beta-endorphin-[1-27] (6 micrograms), but not naloxone (1 microgram).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Different mechanisms mediating tail-flick inhibition induced by beta-endorphin, DAMGO and morphine from ROb and GiA in anesthetized rats. 202 8

1. Modifications by stress of the effects of morphine on pituitary-adrenocortical activity were examined in the guinea-pig at different lengths of time. 2. An increase in plasma cortisol but not in beta-endorphin levels was obtained in guinea-pigs stressed for 60 min. 3. Morphine (50 mg kg i.p.) enhanced beta-endorphin and cortisol levels 5 min after injection and decreased beta-endorphin concentration 30 and 90 min after its administration. 4. In stressed guinea-pigs plasma beta-endorphin levels were reduced 5 min after morphine injection. 5. These results indicate that stress can alter the effects of morphine on pituitary-adrenal activity in the guinea-pig and that the type of modification may be dependent on the time of the sampling.
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PMID:Influence of stress in the effects of morphine on pituitary-adrenocortical activity in the guinea-pig. 205 15

The current study examined the effects of intraperitoneal (IP) and intracisternal (IC) administration of the opiate agonist, morphine, and an opioid, central beta-endorphin, on thyrotropin releasing hormone (TRH)-induced small intestinal transit increases. Anesthetized rats, 14-day and older, were studied to determine age-related differences. Results showed that in all age groups IP morphine (2 mg/kg) blocked TRH (15 micrograms)-induced increases in transit of a charcoal bolus. Morphine 1 microgram and beta-endorphin 1 microgram administered IC in 0.6 microliter failed to block TRH (10 microgram)-induced increases in intestinal transit in 14-day-old rats. However both morphine and beta-endorphin 1 micrograms IC blocked TRH-induced increases in adult rats. Dose-response studies demonstrated that higher doses (greater than 1 microgram) of morphine IC were required to block TRH-induced increases in preweaning rats.
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PMID:Morphine inhibits TRH-induced intestinal transit increases. 212 99

D-Tyr-Ser-Gly-Phe-Leu-Thr (DSLET), beta-endorphin, morphiceptin and morphine were microinjected at 48-h intervals into the amygdala or hippocampus of awake rats in an attempt to identify the opiate receptor types involved in opioid kindling. DSLET, beta-endorphin, morphiceptin and morphine were injected into the lateral ventricle to assess the possibility of kindling seizures by this route. The delta-receptor agonist DSLET effectively kindled convulsions when microinjected into amygdala or ventral hippocampus. The convulsions were suppressed or strongly attenuated by ICI 174,864, a specific antagonist of the delta-receptor, microinjected into the same brain site, but were not affected by ICI 174,864 administered peripherally. When microinjected into amygdala or hippocampus, beta-endorphin and morphiceptin also kindled convulsions, which were antagonized by naloxone but not by ICI 174,864. Morphine evoked EEG epileptiform activity but did not kindle convulsions from limbic brain sites. DSLET occasionally evoked epileptiform spiking and submaximal convulsions when injected into ventricle, and morphiceptin evoked epileptiform spiking only, but tolerance to these effects occurred after repetition of the injections. Thus, convulsions can be kindled by activation of either mu-, delta- or epsilon-receptors when opioids are injected directly into limbic tissue. However, the ability of these compounds to kindle seizures is markedly reduced when they are administered into ventricle. The striking differences between the present results and previous results obtained by peripheral or intraventricular administration of opioid peptides suggest that the route of administration, among other variables, is a crucial factor in assessing the epileptogenic properties of opioid peptides.
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PMID:Involvement of multiple opiate receptors in opioid kindling. 216 33


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