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 specificity of the hypoglycemic response to the intrathecal (i.t.) administration of the naturally occurring (-)-enantiomer of morphine previously reported from our laboratory was studied in mice. (+)-Morphine HBr (50 micrograms) caused a behavioral syndrome (scratching, biting, seizures) comparable to that produced by (-)-morphine sulfate (50 micrograms), but did not cause hypoglycemia. Many opioids, at a dose of 50 micrograms i.t. in nonfasted mice, showed either a saline-like hyperglycemic response or no significant effect on blood glucose. (+)-Morphine, ketocyclazocine, U-50,488, (-)- and (+)-N-allyl-normetazocine, beta-endorphin, (-)- and (+)-naloxone and naltrexone caused hyperglycemia. Significant changes from basal blood glucose were not produced by [D-Pen2, L-Pen5]-enkephalin, [D-Ser2]-Leu-enkephalin-Thr or sufentanil in 50-micrograms doses, or by codeine (300 micrograms), levorphanol (400 micrograms) or methadone (200-400 micrograms). Agonists which produced both hypoglycemic and behavioral effects were, in order of decreasing potency, hydromorphone greater than normorphine greater than morphine greater than 6-acetylmorphine greater than oxymorphone much greater than heroin. Morphine-induced hypoglycemia was partially antagonized by the i.t. coadministration of naloxone methobromide (10 micrograms). Fasting for 24 hr increased the sensitivity to hypoglycemic and lethal effects of morphine. D-Ala2-N-Me-Phe4-Gly5-ol]-enkephalin (5-50 micrograms i.t.) tended to decrease blood glucose in both nonfasted and fasted mice, but these effects were moderate and appeared to be unrelated to dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypoglycemia induced by intrathecal opioids in mice: stereospecificity, drug specificity and effect of fasting. 235 29

The influence of the POMC-system on the effects of morphine during learning are studied using physical (adrenalectomy, stress) and drug impacts (morphine, methamizol, acetysal) on the functional activity of the system. Adrenalectomized rats are found to manifest a sharp rise in the plasma and adenopituitary levels of beta-endorphin and inhibition of learning. The facilitating effect of morphine on learning (in a dose of 5 mg/kg) is inverted against the background of adrenalectomy. Dexamethasone prevents this effect, which coincides with the decrease in the beta-endorphin level. Morphine in a dose of 10 mg/kg body mass enhances learning against the background of stress applied in advance. In unstressed animals the same dose of morphine results in sharp deterioration of learning. Naloxone prevents the positive effect of morphine under stress. The dose-dependent opposite effects of morphine on the processes of learning are assumed to be modulated by the changes taking place in the ratio of the opioid/antiopioid POMC-derivatives under functional and drug influences.
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PMID:Participation of the POMC-system in the effects of morphine on the avoidance reaction in albino rats. 239 49

The effects of locally applied opioids on the release of immunoreactive Substance P (iSP), induced by mechanical stimuli, from the dorsal horn of the rabbit in situ, were investigated. Morphine and met-enkephalin (met-enk), but not dynorphin A (1-17) (DYN), in a concentration of 10 microM, significantly inhibited the evoked release. These inhibitory effects of morphine and met-enkephalin were antagonized by the local application of naloxone (10 microM) to the dorsal horn. These results suggest that the inhibition of the release of Substance P induced by noxious mechanical stimuli may be mediated by mu and delta, but not by kappa opioid receptors.
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PMID:Met-enkephalin and morphine but not dynorphin inhibit noxious stimuli-induced release of substance P from rabbit dorsal horn in situ. 241 Aug 7

We have reported previously that i.v.t. beta-endorphin increases the release of immunoreactive Met-enkephalin but not Leuenkephalin or dynorphins from the spinal cord. To determine if the effect is specific to beta-endorphin, the present investigation tested i.v.t. beta-endorphin, its analogs and other opiate agonists with different opioid receptor activities for their ability to release Met-enkephalin using an intrathecal perfusion technique. Human beta-endorphin and its analogs, human beta-endorphin-(1-30), -(1-29) and -(1-28) which have an identical amino acid sequence in the NH2-terminus showed reduced stepwise potencies in releasing Met-enkephalin. The results correlated well with their analgesic potencies. Des-Met5-camel beta-endorphin (64 micrograms i.v.t.) which does not have a complete sequence of Met-enkephalin in its NH2-terminus but still retains 20% of camel beta-endorphin analgesic potency caused the spinal release of Met-enkephalin. Morphine (mu opioid receptor agonist, 40 micrograms), D-Ala2-D-Leu5-enkephalin (delta opioid receptor agonist, 80 micrograms) and U-50488H (kappa opioid receptor agonist, 160 micrograms) injected i.v.t. were unable to cause any release of Met-enkephalin. High-performance liquid chromatography after Sephadex G-50 gel chromatography indicated that the immunoreactive Met-enkephalin in the spinal perfusate released by i.v.t. beta-endorphin had a retention time identical to authentic Met-enkephalin. Intraventricular injection of Met-enkephalin, 4 nmol (2.3 micrograms), caused little increase of Met-enkephalin immunoreactivity in the spinal perfusate, whereas 4 nmol of i.v.t. beta-endorphin caused a marked increase of Met-enkephalin in the spinal perfusate. Inhibition of peptidase by i.v.t. aprotinin and bacitracin does not prevent the spinal release of Met-enkephalin induced by i.v.t. beta-endorphin. It is concluded that the release of Met-enkephalin was specific to beta-endorphin and the results were not due to cross-immunoreactivity of beta-endorphin or its metabolites.
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PMID:Spinal release of immunoreactive Met-enkephalin by intraventricular beta-endorphin and its analogs in anesthetized rats. 242 Sep 69

The present study was aimed to examine possible influences of bradykinin (BK) and substance P (SP) on met-enkephalin (ME)-like peptide content in the rat incisor pulp. Des-Arg9-[Leu8]-BK, a potent BK-antagonist, significantly reduced the increased content of ME-like peptides induced by noxious stimulation, while the effect of BK-antagonist was reversed in combination with BK. Morphine decreased the increased content of ME-like peptides. Ethylketocyclazocine, a kappa-agonist, also decreased the increased content of the peptides. From these results, it was suggested that BK might be a trigger in the increase of ME-like peptide content induced by noxious stimulation and, in contrast, ME-like peptides in the pulp might inhibit BK release from the pulp in a negative feedback mechanism. On the other hand, [D-Pro2,D-Trp7,9]-SP, a potent SP-antagonist, did not show any significant influence to ME-like peptide content in the pulp. Furthermore, the content was not changed following cutting of inferior alveolar nerve. From these results, it was suggested that ME-like peptides in the pulp cells might be independent on SP-containing nerves in the pulp.
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PMID:Influences of bradykinin and substance P on the met-enkephalin-like peptide content in the rat incisor pulp. 242 25

1. The effects of intravenous (i.v.) morphine on adrenocorticotrophic hormone (ACTH), beta-endorphin (beta-END), total catecholamines (CA) and histamine (HIS) plasma concentrations, were determined in anaesthetized dogs at 30 degrees C and 37 degrees C. 2. Hypothermia initially increased CA levels by 29%, but the values returned to baseline after 2 h. Morphine (1 mg/kg, i.v.) produced a significant decrease in CA both at 37 degrees C and 30 degrees C (34% and 54%, respectively). Subsequent administration of naloxone (1 mg/kg, i.v.) significantly increased CA levels in both groups. 3. Hypothermia per se had no effect on ACTH, beta-END, and HIS concentrations. Morphine produced a significant increase in pituitary hormones and HIS, in hypothermic but not in normothermic animals. Morphine concentrations were significantly higher at 30 degrees C during the first 45 min. 4. The results suggest that the effects of morphine on hormonal and histamine release observed at 30 degrees C are concentration-dependent and related to changes in morphine pharmacokinetics.
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PMID:Hypothermia enhances the effects of morphine on hormonal and histamine release. 247 84

Beta-endorphin (0.7 and 2.8 mg/kg) and morphine (0.15 and 0.60 mg/kg) were administered intravenously to rhesus monkeys responding on an operant schedule. Beta-endorphin injections resulted in dose-dependent effects which included marked, but relatively brief disruptions in behavioral responding, decreases in systolic blood pressure, and more protracted increases in heart rate. Morphine injections were followed by much longer duration decreases in response rates and systolic blood pressure, and an irregular but largely deceleratory heart rate response. On a molar basis, beta-endorphin was approximately twice as potent as morphine. It was concluded that intravenously administered beta-endorphin exerts behavioral and physiological effects in the unanesthetized primate.
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PMID:Intravenous beta-endorphin: behavioral and physiological effects in conscious monkeys. 253 74

Effects of leu- and met-enkephalin, pentazocine and morphine on negative or positive chronotropic response to vagal nerve stimulation or cardiac sympathetic nerve stimulation were examined in anesthetized dogs in order to determine whether opioid receptors modulate vagal and sympathetic transmission. Leu- and met-enkephalin (10-100 micrograms/kg i.v.) and pentazocine (100-1000 micrograms/kg i.v.) inhibited bradycardic response to vagal nerve stimulation (1-4 Hz) in a dose-dependent manner. Morphine (300 and 1000 micrograms/kg i.v.) did not affect vagal bradycardia. The inhibitory effect of leu-enkephalin (30 micrograms/kg) and pentazocine (300 micrograms/kg) was effectively antagonized by naloxone (1000 micrograms/kg i.v.). Bradycardic response to intracoronary injection of methacholine (0.1, 0.3 and 1 microgram) into the right coronary artery was unaffected by leu-enkephalin (30 micrograms/kg). On the other hand, leu-enkephalin and pentazocine did not modify tachycardic response to sympathetic nerve stimulation (1-8 Hz). Morphine attenuated sympathetic tachycardia only slightly. These results suggest that presynaptic opioid receptors, probably delta type, are present in the vagus nerves, and that the activation of opioid receptors inhibit vagal transmission to the dog heart. In contrast, the presence of opioid receptors in the cardiac sympathetic nerves is not evident.
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PMID:Effects of opioid agonists on sympathetic and parasympathetic transmission to the dog heart. 255 Jun 14

Exogenously applied opioid agonists have a stimulatory effect on adrenocorticotropic hormone (ACTH) secretion. The present experiments were designed to examine the mechanisms involved in the stimulatory effect of the mu-receptor agonist morphine on ACTH release in chronically cannulated, freely moving, non-stressed rats. Morphine (7.5 mg/kg, i.v.) treatment was followed by a significant increase in plasma levels of ACTH. Pretreatment with the peripheral ganglionic blocker chlorisondamine (3 mg/kg, i.p.) attenuated the response to morphine. The morphine stimulatory effect was also partially inhibited if the rats were pretreated with a specific antiserum to corticotropin-releasing factor (CRF). In rats given both CRF antiserum and chlorisondamine, the plasma ACTH levels remained unchanged after morphine application. These findings indicate that morphine stimulates the release of ACTH by activating both CRF-secretion and peripheral sympathetic neuronal pathways.
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PMID:Facilitation of ACTH secretion by morphine is mediated by activation of CRF releasing neurons and sympathetic neuronal pathways. 255 64

In order to evaluate the regulation of neuropeptide stores in structures of the rat brain, the content of the specific messenger ribonucleic acid for the peptide precursor, of the precursor and of its biologically active peptide fragment, resulting from the precursor processing was measured. Enkephalin stores of the striatum, but not that of other structures, were upregulated by repeated daily doses of dopaminergic receptor antagonists of the D-1 type. Morphine tolerance failed to change stores of enkephalin in brain but produced a down-regulation of the synthesis of pro-opiomelanocortin in the hypothalamus. The regulation of diazepam binding inhibitor (DBI), the precursor of a family of putative endogenous ligands of the benzodiazepine recognition site, was studied during tolerance to benzodiazepines. Tolerance to diazepam increased the dynamic state of an octadecaneuropeptide (ODN), derived from DBI, in the cerebellum and cortex. The steady state or dynamic state of ODN were not changed in other structures of the brain of the rat, tolerant to diazepam.
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PMID:In vivo studies of the regulation of neuropeptide stores in structures of the rat brain. 282 28


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