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)

Morphine (1,0 mg/kg), ACTH1-24 (10.0 micrograms/kg), epinephrine (12.0 micrograms/kg), Met-enkephalin (2.0 and 5.0 micrograms/kg), Leu-enkephalin (2.0 micrograms/kg) and des-Tyr-Met-enkephalin (2.0 micrograms/kg) all produced marked reductions of beta-endorphin-like immunoreactivity in the rat diencephalon. At a dose of 0.4 mg/kg, naloxone had no effect of its own and was unable to reverse the depleting effect of the other substances. The depletion of beta-endorphin-like immunoreactivity caused by the various treatments is attributable to release and subsequent degradation of beta-endorphin and/or of its precursors. The various behavioral effects of morphine, ACTH, epinephrine and the enkephalins may be explained by the release of endogenous beta-endorphin.
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PMID:Effect of morphine, ACTH, epinephrine, Met-, Leu- and des-Tyr-Met-enkephalin on beta-endorphin-like immunoreactivity of rat brain. 629 17

Morphine given systemically or centrally increases the plasma concentration of cyclic GMP in male, ddY strain mice. Normorphine also increased the plasma cyclic GMP level, whereas the same dose of ketocyclazocine and SKF 10,047 had no effect. The effect of morphine on plasma cyclic GMP was mimicked by opioid peptides such as (D-Ala2, Met)-enkephalinamide, FK 33,824 or beta-endorphin. The effect of morphine and opioid peptides on plasma cyclic GMP was antagonized by naloxone, indicating the involvement of the opiate receptor. The increase in plasma cyclic GMP elicited by morphine was abolished by vagotomy and pretreatment with hexamethonium and atropine and was partly inhibited by pretreatment with phentolamine. Adrenalectomy and pretreatment with propranolol, which inhibited the increase in plasma cyclic AMP level elicited by morphine (Muraki et al., 1979), did not alter the cyclic GMP response to morphine. The development of tolerance to the cyclic GMP increase was observed in morphine-tolerant/dependent mice. These results suggest that morphine increases the plasma cyclic GMP level by activating the preganglionic parasympathetic tone via the stimulation of the opiate receptors, thereby increasing the generation of cyclic GMP through the muscarinic receptors on the effector cells.
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PMID:Mechanism of morphine in increasing plasma cyclic GMP level in male mice. 629 63

The roles of corticotropin and morphine in the regulation of phosphofructokinase (PFK) activity in rat mammary glands were investigated by the administration of corticotropin, morphine and dexamethasone. Corticotropin increased the activity of PFK in the mammary glands of intact and hypophysectomised animals but was without any effect in tissues from ovariectomised and adrenalectomised animals. Morphine administration resulted in a significant decrease in the enzyme's activity in intact animals only. A combined dose of corticotropin and morphine significantly reduced the corticotropin-induced increase in the activity in both intact and hypophysectomised animals. Dexamethasone treatment resulted in a significant increase in the activity in hypophysectomised and ovariectomised plus adrenalectomised animals and morphine was able to reduce the glucocorticoid-induced rise. It is postulated that endogenous opioids might be playing a dual role in the regulation of glycolysis by inhibiting the release of corticotropin and regulating the action of glucocorticoids at the cellular level in the mammary gland.
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PMID:Corticotropin and morphine interaction in the regulation of phosphofructokinase activity in rat mammary gland. 630 62

The purpose of this study was to investigate the effect of oral administration of progesterone (15 micrograms norethindrone, NE) in presence and absence of estradiol (1 microgram ethinyl estradiol, EE2) on the CNS levels of beta-endorphin like immunoreactivity (beta-EI) in female rats. In acute study (5 days), NE alone did not change beta-EI significantly in pituitary. NE and EE2 together decreased beta-EI by 37% (47% at 10X dose). In chronic study (7 weeks), 2NE had no significant effect on pituitary beta-EI, however, NE and EE2 together at 10X dose decreased it by 14%. In the hypothalamus, NE alone or in presence of EE2 had no significant effect on beta-EI, but 10X dose of NE+ EE2 caused 50 and 76% decrease in beta-EI in acute and chronic study. Striatum was the only tissue where NE alone caused a decrease of 82% in beta-EI when given acutely and 52% when given chronically. EE2 had some protective effect on this decrease since when given together (NE+EE2) the decrease in beta-EI was 21% in acute and 43% in chronic study. Thus our results, along with other studies on the regulation of gonadotropin levels by opioids, suggest that oral contraceptives alter the level of beta-EI and in turn may regulate the release of gonadotropins. Morphine and endogenous opioids have been shown to decrease gonadotropin secretion in various species including humans, apparently by suppressing the release of LH-RH from the hypothalamus (1-5). The opiate antagonist naloxone not only causes up to 10-fold increase in the secretion of gonadotropins (1,3, 6-9) but also opposes the negative feedback effect of steroids on the hypothalamic-pituitary-gonadotropin axis (8), suggesting a regulatory interaction between the endogenous opioids, gonadotropins and gonadal steroids. Like ACTH, the secretion of beta-endorphin is inhibited by glucocorticoids (10). Naloxone induced release of LH is facilitated by estradiol in humans (11) suggesting an antagonistic effect of estradiol on the endogenous opioids. beta-endorphin may play a significant role in neurochemical mechanisms of gonadotropin release in the human menstrual cycle. A preovulatory increase of beta-endorphin in serum occurs 2 days prior to LH surge and a postovulatory decrease in beta-endorphin occurs 5 days later.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of oral contraceptives on the rat brain and pituitary beta-endorphin. 631 7

Rat erythrocyte ghosts containing 45Ca++, EGTA, ATP and Pipes buffer (pH 7.2) were prepared for studying opioid effects on Ca++ flux. Ethylketocyclazocine and dynorphin 1-13 (dynorphin) dose-dependently inhibited La+++-sensitive outward 45Ca++ movement at nM concentrations and the effect was naloxone reversible. Morphine and beta-endorphin were also effective at higher concentrations, whereas levorphanol and leu-enkephalin were ineffective. None of the opioids studied inhibited 45Ca++ inward movement. Based on these findings, it is concluded that rat erythrocyte possesses k-type opioid receptors through which the Ca++-pump may be inhibited.
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PMID:Possible inhibition of Ca++ pump of rat erythrocyte ghosts by opioid k agonists. 631 22

The effects of repeated infusion of small, initially subconvulsive amounts of beta-endorphin, met-enkephalin or morphine sulfate into the amygdala and hippocampus were investigated. beta-endorphin and met-enkephalin evoked epileptiform spiking when infused into the posterior amygdala or ventral hippocampus. Morphine evoked epileptiform spiking when infused into the anterior amygdala. Naloxone blocked or terminated the spiking. Repetition of the infusions led to the gradual development of bilateral generalized convulsions by beta-endorphin and met-enkephalin and to the development of tolerance to morphine. An unexpected observation was that handling, immobilization or conspecific threat potentiated the epileptiform effects of beta-endorphin and morphine in many cases. These results suggest that endogenous opiate mechanisms might play a role in convulsive seizures and that stressful stimuli can exacerbate opiate seizures.
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PMID:Intracerebral beta-endorphin, met-enkephalin and morphine: kindling of seizures and handling-induced potentiation of epileptiform effects. 632 69

Opioid agonists were used to investigate the modulation of seizures mediated by mu, kappa and delta opiate receptors in the seizure-sensitive Mongolian gerbil. Morphine (1.0-25 mg/kg, s.c.) were used as prototypic agonists for mu, kappa and delta opiate receptors. Each opioid decreased the incidence and severity of the seizure as compared to control values. The anticonvulsant effects of morphine (10 mg/kg, s.c.) and ketocyclazocine (0.5 mg/kg, s.c.) were reversed by naloxone (1.0 mg/kg, s.c.), while the anticonvulsant effects of N-allylnormetazocine (2 mg/kg, s.c.) were not significantly changed by naloxone. Additionally, abnormal behavior was observed following administration of the opioids. Morphine (10 mg/kg, s.c.) produced excitation and hyperresponsiveness with intermittent cataleptic-like states. Ketocyclazocine (10 mg/kg, s.c.) predominantly produced a stuporous, immobile state, accompanied by some loss of posture. N-allylnormetazocine (10 mg/kg, s.c.) produced ataxia and stereotypic side-to-side head nodding . Naloxone was able to reverse the behavioral effects produced by morphine and ketocyclazocine but not those produced by N-allylnormetazocine. The data presented are consistent with earlier studies which demonstrated the anticonvulsant effects of beta-endorphin in the gerbil. This study further suggests that opioids have a protective role against seizure activity in the gerbil and the opioid anticonvulsant effect is not specific to one type of opioid agonist.
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PMID:Similar anticonvulsant, but unique, behavioural effects of opioid agonists in the seizure-sensitive Mongolian gerbil. 633 Jun 6

Morphine, beta-endorphin and [D-Ala2, D-Leu5] enkephalin administered intracerebroventricularly exerted a protective effect on electroconvulsive shock (ECS)-induced seizures in mice. This effect was reversed by intraperitoneal injections of naltrexone. The role of mu and delta receptors in ECS-induced convulsions is discussed.
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PMID:Opioid antagonism of electroshock-induced seizures. 633 Jul 66

Neonatal administration of monosodium glutamate (MSG) destroyed perikarya in the arcuate nucleus and median eminence, including those that contain met-enkephalin and beta-endorphin and it increased the density of opiate receptors in the midbrain. Treatment with glutamate decreased the analgesic response on the jump test following a 10 mg/kg dose of morphine, yet increased the analgesic response on the hot-plate test following 1 mg/kg dose of morphine. The present study demonstrated that changes in morphine-induced analgesia induced by glutamate varied as functions of the pain test and of gender. While males treated with glutamate displayed attenuated analgesia induced by morphine (2.5-15 mg/kg) on the jump test, jump thresholds of females treated with glutamate were potentiated after a 10 mg/kg dose of morphine and attenuated after a 15 mg/kg dose of morphine, relative to controls. In contrast, analgesia on the hot-plate test was potentiated in animals of both genders treated with glutamate after all doses of morphine. Changes in tolerance to morphine induced by glutamate also depended on the pain test and gender. While the peak analgesic response on the jump test did not occur until the fifth injection of morphine in all rats treated with glutamate, tolerance on the jump test was subsequently retarded in males treated with glutamate and accelerated in glutamate-treated females. Tolerance on the hot-palate test appeared not to be consistently affected by treatment with glutamate. Morphine-induced hyperthermia was initially decreased in rats treated with glutamate, but subsequently decreased in glutamate-treated males and increased in glutamate-treated females.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Monosodium glutamate and analgesia induced by morphine. Test-specific effects. 652 50

In order to investigate the opiate receptors involved in the control of anterior pituitary hormone secretion, five different opioid drugs were administered intravenously to groups of 6 normal male subjects. Morphine (10 mg), methadone (10 mg), pentazocine (30 mg), nalorphine (10 mg) and 0.25 mg of the met-enkephalin analogue, DAMME, all caused similar increases in circulating prolactin with falls in serum LH and cortisol. Methadone and DAMME also elevated GH and TSH; morphine elevated TSH but not GH, nalorphine GH but not TSH. After pentazocine neither GH nor TSH changed. FSH failed to change significantly after any drug. All these changes, except serum cortisol, were antagonised by 4 mg naloxone. Taking into account the known receptor subtypes preferentially activated by each opiate, it is suggested that prolactin secretion is modulated by epsilon-receptors and TSH by mu-receptors. The control of ACTH probably involves delta-or kappa-receptors, that for LH kappa-or epsilon-receptors. It is not possible on present data to allocate a specific receptor mediating the opioid control of GH.
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PMID:Differential effects of opiate peptides and alkaloids on anterior pituitary hormone secretion. 663 17


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