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)

To determine the locus of opiate modulation of ACTH secretion, 11 normal subjects were given ovine corticotropin-releasing hormone (CRH) 30 min after receiving either placebo or morphine sulfate. Plasma ACTH, cortisol, arginine vasopressin (AVP), epinephrine, norepinephrine, and CRH were measured 30 min before and up to 150 min after CRH administration. Morphine blunted the ACTH response for the first 60 min and cortisol response for the first 90 min after CRH administration. Morphine did not lower arginine vasopressin or catecholamine levels. To determine whether morphine's effect on ACTH and cortisol was due to a direct action on the corticotroph cell, dispersed rat pituitary cells were perifused with medium containing 1 microgram/ml morphine sulfate or medium alone. Morphine had no effect on the ACTH response of these cells to 10 nM CRH pulses. Similarly, morphine had no effect on ACTH production by dispersed rat pituitary cells in monolayer culture in response to 90- and 180-min incubations with 5 nM CRH. We conclude that morphine blunts the early response of the pituitary gland to CRH in vivo. Based on the lack of a direct effect of morphine on rat pituitary cells in vitro, we postulate that morphine given in vivo may modulate the pituitary ACTH response to CRH through other suprapituitary factors.
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PMID:Morphine inhibits the pituitary-adrenal response to ovine corticotropin-releasing hormone in normal subjects. 298 35

The effects of agents representing three classes of benzodiazepine receptor-acting drugs on circulating levels of beta-endorphin-like immunoreactivity (beta-END-LI) were examined in male rats. The active benzodiazepine receptor antagonists, ethyl-beta-carboline-3-carboxylate (beta-CCE, 30 mg/kg), methyl-beta-carboline-3-carboxylate (3 mg/kg), and 2-phenylpyrazolo [4,3-c]quinolin-3(5H)-one (CGS-8216, 3 mg/kg), all evoked 3- to 4-fold increases in plasma levels of beta-END-LI as compared to control values. The beta-CCE-induced rise in circulating beta-END-LI was significantly attenuated by pretreatment with the agonist diazepam (2.5 mg/kg) and the antagonist ethyl-8-fluoro-5,6-dihydro-5-methyl-6-oxo-4H-imidazo-[1,5-alpha] [1,4]benzodiazepine-3-carboxylate (Ro 15-1788, 10 mg/kg) but was unaltered by morphine (1 and 5 mg/kg). Ro 15-1788 also significantly attenuated the methyl-beta-carboline-3-carboxylate- and CGS-8216-induced release of pituitary beta-END-LI in vivo. Morphine (5 mg/kg) and diazepam (5 mg/kg) together, but neither alone, significantly reduced the rise in plasma beta-END-LI due to physical immobilization or foot shock. Pretreatment with dexamethasone (100 micrograms), an inhibitor of pituitary anterior lobe (AL) beta-END-LI secretion, completely prevented the plasma beta-END-LI increase due to beta-CCE. Chromatographic analysis of plasma beta-END-LI revealed that most of the beta-END-LI secreted in response to beta-CCE and CGS-8216 resembles beta-lipotropin (beta-LPH), a marker for beta-END-LI release from the AL, in molecular size. Results of in vitro studies indicate that the effects of the anxiogenic agents, beta-CCE and CGS-8216, on AL beta-END-LI release in vivo were not mediated by direct actions of these agents on the pituitary gland. Together, these findings suggest that an interaction exists between a benzodiazepine receptor mechanism(s) and regulation of hypothalamic corticotropin-releasing factor(s) which in turn controls beta-END-LI secretion from the AL of the rat pituitary gland.
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PMID:Evidence that a benzodiazepine receptor mechanism regulates the secretion of pituitary beta-endorphin in rats. 299 Aug 51

It is suggested that the antipsychotic efficacy of opioids in patients suffering from schizophrenia may result from an interaction of opioids with the dopaminergic system. The modulatory effect of opioids on dopaminergic functions has already been demonstrated in basic experiments: Anatomical and biochemical data reveal an interaction between opioid receptors and dopamine (DA) actions on dopaminergic nerve terminals, cell bodies, and afferent nerve endings. Endogenous enkephalin levels correlate well with the endogenous dopamine content in various brain areas. Systemic or iontophoretic administration of morphine alters the spontaneous activity of ventral tegmental dopaminergic neurons. Morphine and enkephalin effectively enhance pituitary prolactin release, whereas dopamine inhibits it. Opioid agonists effectively alter DA release, DA reuptake, and DA metabolism in the striatum and substantia nigra. In reverse, chronic neuroleptic treatment enhances the synthesis and release of pituitary beta-endorphin. Opioids affect contralateral rotation elicited by dopamine agonists in animals with unilateral lesions of the nigrostriatal pathway. Phencyclidine, a psychotropic drug that shares certain pharmacological characteristics with the putative sigma-opioid receptor ligand SKF 10,047, indirectly mimics the effects of dopamine agonists on prolactin release, release of acetylcholine, etc. It is suggested that an imbalance of opiate-DA interaction might be involved in the pathogenesis of schizophrenia. Consequently, clinical studies on the effects of opioids on psychotic symptoms should also examine opioid influence on dopaminergic functions in these patients.
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PMID:Dopamine and the action of opiates: a reevaluation of the dopamine hypothesis of schizophrenia. With special consideration of the role of endogenous opioids in the pathogenesis of schizophrenia. 299 42

Methionine enkephalin, leucine enkephalin, [D-Ala2, D-Leu5] enkephalin, alpha-neoendorphin, beta-endorphin, dynorphin (1-13) and ethylketocyclazocine inhibited the contractions of rabbit ear artery ring segments elicited by transmural nerve stimulation at 8 Hz. Ethylketocyclazocine, dynorphin (1-13) and leucine enkephalin produced partial inhibition, their apparent intrinsic activities (alpha) being 0.57, 0.75 and 0.66, respectively. Morphine and normorphine, which are agonists at mu-receptors, did not inhibit the response of the artery. Naloxone antagonized the actions of opioids and ethylketocyclazocine, and was more effective against methionine enkephalin, leucine enkephalin and [D-Ala2, D-Leu5] enkephalin than against alpha-neoendorphin, ethylketocyclazocine and dynorphin (1-13). The pA2 values of naloxone against so-called delta-agonists were approx. 8.5, and against so-called kappa-agonists were approx. 7.7. The supposed kappa-antagonist, Mr2266, was more effective than naloxone in antagonizing the actions of alpha-neoendorphin, and the kappa-agonists dynorphin (1-13) and ethylketocyclazocine. The pA2 values of Mr2266 against kappa-agonists were 8.5-9.0, and against delta-agonists were 7.8 or less. The opioid peptides and opioids tested did not cause dilatation of the artery previously contracted with histamine. These results suggest that the opioid peptides and ethylketocyclazocine acted on opioid receptors at adrenergic nerve terminals in the ear artery. The opioid receptors appear to be of the delta- and kappa-types, not the mu-type.
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PMID:Opioid receptor types on adrenergic nerve terminals of rabbit ear artery. 299 21

Secretion of HCO3- by duodenum just distal to the Brunner's glands area and devoid of pancreatic HCO3- was titrated in situ in anesthetized rats. Secretion increased significantly after intravenous injection of small amounts (10-20 ng/kg) of the opioid peptides beta-endorphin, methionine-enkephalin, and leucine-enkephalin. Maximum (approximately twofold) stimulation by beta-endorphin and leucine-enkephalin occurred at 20 ng/kg. Morphine (50 micrograms/kg) caused a similar stimulation and the mu-selective opiate antagonist naloxone prevented the stimulation by beta-endorphin and morphine. The synthetic analogue [D-Ala2,D-Leu5]-enkephalin (500 ng/kg), which is an agonist primarily at delta-opiate receptors, had no effect, further suggesting that the stimulation of duodenal HCO3- secretion is mediated by mu-receptors. Naloxone alone did not affect basal HCO3- secretion but reduced the duration of the rise in secretion in response to a 5-min exposure to luminal acid (pH 2.00). Endogenous opioid peptides may thus have a role in the humoral or neural control, or both, of duodenal surface epithelial HCO3- secretion and mucosal protection.
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PMID:beta-Endorphin and enkephalins stimulate duodenal mucosal alkaline secretion in the rat in vivo. 300 Aug 61

The hormonal and neurochemical responses to acute ether stress, morphine, and/or naloxone were analyzed in infantile (13-day-old) and prepubertal (36-day-old) male CD rats in an attempt to identify a possible neurochemical correlate(s) for the previously demonstrated requisite maturation of the PRL response to ether stress. Neuronal serotonin (5-HT), norepinephrine (NE), and dopamine (DA) activities were examined in the medial preoptic hypothalamic area (MPOH), medial basal hypothalamic area (MBH), and median eminence (ME). Ether stress increased plasma PRL, ACTH, and beta-endorphin-like immunoreactivity (beta end) as well as NE metabolism in the MPOH and MBH and neuronal 5-HT activity in the MBH, and decreased neuronal DA activity in the ME of prepubertal animals. Ether stress elicited similar changes in infantile animals, with the important exceptions that plasma PRL, neuronal 5-HT activity in the MBH, and neuronal DA synthesis in the ME were not affected at this earlier age. Morphine increased plasma PRL, ACTH, and beta end levels, elevated neuronal NE and 5-HT activities in the MPOH and MBH, and decreased DA synthesis in the ME in both infantile and prepubertal animals. Naloxone administration did not alter basal hormone concentrations or neuronal monoamine activity in any brain area, but did prevent all of the morphine-induced changes as well as the ether stress-induced changes in PRL, MBH neuronal 5-HT activity, and DA synthesis in the ME of prepubertal animals. In addition, naloxone augmented the ether stress-induced increases in ACTH and beta end in prepubertal rats. Indirect stimulation of 5-HT neurons by administration of the amino acid precursor of 5-HT, 5-hydroxytryptophan, resulted in decreased DA synthesis in the ME of infantile animals and increased plasma PRL levels in that age group, indicating that this portion of the neurochemical connection is already present in infantile animals. Furthermore, the 5-hydroxytryptophan-induced increase in PRL was blocked by pretreatment with naloxone. The results demonstrate that both the ether stress- and morphine-induced increases in plasma PRL, but not in ACTH or beta end, are associated with increased neuronal 5-HT activity in the MBH and a decreased neuronal DA activity in the ME, that these are opiate receptor-mediated effects, and that infantile rats apparently lack a functional opiate-5-HT connection, which matures some time between days 13 and 36 postnatally.
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PMID:Maturation of the prolactin and proopiomelanocortin-derived peptide responses to ether stress and morphine: neurochemical analysis. 300 67

The activity of adenylate cyclase in striatal membrane-enriched fractions (25,000 g) was inhibited by morphine, beta-endorphin, [D-Ala2-D-Leu5] enkephalin (DADLenk), fentanyl and bremazocine. Whereas guanosine triphosphate (GTP) appeared essential for the expression of this effect, sodium chloride seemed to enhance the degree of inhibition. Dopamine stimulation and sodium fluoride activation of the enzyme was also suppressed by morphine, beta-endorphin and DADLenk. beta-Endorphin and DADLenk inhibited adenylate cyclase activity in vasa deferentia membrane-enriched fractions (25,000 g); both opioids required GTP and NaCl and were inhibited by a delta-opioid receptor antagonist and by naloxone. Morphine, bremazocine and tifluadom did not significantly alter the activity of the vas deferens enzyme. Basal cyclic AMP values of striatal slices were not significantly altered by morphine, beta-endorphin or DADLenk. However, dopamine-induced elevation of cyclic AMP was reduced by morphine and this effect of the opiate was suppressed by naloxone. Only beta-endorphin lowered the basal cyclic AMP values in the vas deferens. The physiological relevance of adenylate cyclase coupling to opioid receptor subtypes is considered.
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PMID:Opioid inhibition of adenylate cyclase in the striatum and vas deferens of the rat. 302 42

The occurrence of cross-tolerance between morphine and met-enkephalin, and between morphine and DADL (D-Ala-D-Leu-enkephalin) in causing mydriasis in mice was studied. Morphine-tolerant mice treated with met-enkephalin or DADL intracerebroventricularly (ICV) showed marked reduction of the pupillary effect of the endopioids. Maximal mydriasis in tolerant animals was only about 30% for met-enkephalin and 50% for DADL, compared to levels in nontolerant animals. These results are among the first to demonstrate cross-tolerance between morphine and enkephalins in intact animals and may suggest involvement of multiple opiate receptor systems in producing mydriasis.
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PMID:Opioid mydriasis: cross-tolerance between morphine and enkephalins. 352 Jun 6

The study investigated the interaction between phencyclidine (PCP) and morphine in affecting the levels of met-enkephalin, dopamine, DOPAC and HVA in mice. Morphine 5 mg/kg alone and PCP 10 mg/kg alone failed to change the levels of met-enkephalin in the midbrain and striatum. However, PCP in combination with morphine produced an increase in met-enkephalin levels and a decrease in HVA levels. In the midbrain, there was a direct relationship between the decrease in met-enkephalin levels and the increase in HVA levels. These results suggest that PCP may change the function in dopaminergic and enkephalinergic neuronal systems in the midbrain and/or striatum.
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PMID:Effects of phencyclidine in combination with morphine on the levels of met-enkephalin, dopamine, DOPAC and HVA in discrete brain areas of mice. 383 60

Bicarbonate secretion by 12 mm segments of duodenum just distal to the Brunner's glands area and devoid of pancreatic bicarbonate was titrated in situ in anaesthetised rats. The secretion increased significantly after intravenous injection of small amounts (20 ng/kg) of the endogenous opioid peptides beta-endorphin and methionine enkephalin and maximal (approximately twofold) stimulation occurred after 200-500 ng/kg. Morphine (50 micrograms/kg) caused a similar stimulation and the mu-opiate antagonist naloxone prevented stimulation by morphine. The synthetic analogue [D-Ala2, D-Leu5]-enkephalin (500 ng/kg) which is an agonist at delta-opiate receptors, did not affect the secretion, further suggesting that stimulation is mediated by mu-receptors. VIP (5-100 micrograms/kg) increased the secretion dose-dependently to levels considerably higher than those observed with opiates, and pretreatment with atropine or indomethacin did not affect the response to VIP. The results suggest a role of endogenous opioid peptides and VIP in the humoral and/or nervous control of duodenal surface epithelial bicarbonate secretion and mucosal protection.
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PMID:Effects of some opiates and vasoactive intestinal peptide (VIP) on duodenal surface epithelial bicarbonate secretion in the rat. 386 Sep 26


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