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 effects of angiotensin II (A-II) and corticotropin (ACTH) on insulin-like growth factor-I (IGF-I) receptors of bovine adrenocortical cells were investigated. Pretreatment of cells for 48 h with ACTH or A-II induced in a dose-dependent manner an increase in [125I]IGF-I binding (ED50 congruent to 10(-11)M, Vmax = 10(-10) M with ACTH; ED50 congruent to 3.10(-9) M, Vmax = 10(-7) M with A-II). This resulted from an increase in the number of binding sites without modification of the binding affinity. Pretreatment with 8-Bromo-cAMP (10(-3) M), a phorbol ester (PMA 10(-7) M) + ionophore A23187 (10(-7) M) produced a positive regulation of IGF-I receptors. Glucocorticoids did not mediate the effect of A-II and ACTH on IGF-I receptors. Since previous studies have shown that IGF-I increased ACTH and A-II receptors the present data indicate the existence of a reciprocal positive trophic effect between IGF-I and the two hormones on the regulation of their specific membrane-bound receptors.
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PMID:Regulation of IGF-I receptors by corticotropin and angiotensin-II in cultured bovine adrenocortical cells. 254 91

Adrenocorticotropic hormone (ACTH), while having negligible effects on cardiovascular function in the intact animal, induces a potent and sustained reversal of an otherwise invariably, rapidly fatal condition of hemorrhage-induced hypovolemic shock, in rats and dogs. The main site(s) of action are at the peripheral level; however, subsidiary site(s) of action in the CNS cannot be excluded. The studies on the mechanism of action indicate that the ACTH-induced reversal of hemorrhagic shock (a) is an extra-hormonal, adrenal-independent effect, because it is not affected by adrenalectomy and is shared by many ACTH-fragments practically devoid of corticotropic activity; (b) is antagonized by morphine in a surmontable way; (c) needs the functional integrity of the sympathetic nervous system (it is prevented by guanethidine, reserpine, and clonidine) and the availability of peripheral alpha-adrenoceptors (it is antagonized by dibenamine, prazosin and yohimbine, but not by practolol); (d) requires the integrity of afferent vagal fibers (it is almost completely abolished by vagotomy); (e) involves central cholinergic networks (it is antagonized by atropine sulphate, but not by atropine methyl bromide; and it is prevented by the intracerebroventricular injection of hemicholinium-3); (f) is associated with a massive increase in the volume of circulating blood, likely due to a mobilization from peripheral pooling sites (it is largely prevented by splenectomy or by suprahepatic veins ligature, and is associated with a restoration of the venous blood flow in peripheral vascular beds and with a normalization of venous PO2); (g) is associated with a restoration of heart and spleen adrenoceptors, whose number is significantly decreased during hemorrhagic shock. The survival time of hemorrhage-shocked animals, which is 26 +/- 3 min in controls, is greatly prolonged (44 +/- 18 h) by ACTH, provided that the treatment is made within 5-10 min after bleeding. Finally, in animals treated with ACTH within 5-10 min after bleeding, blood reinfusion retains its effectiveness and reverse shock even if performed 2-5 h later.
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PMID:The adrenocorticotropic hormone (ACTH)-induced reversal of hemorrhagic shock. 255 78

Pentylenetetrazol (PTZ, 45 mg/kg, ip) impaired retention of a one-trial step-through inhibitory avoidance task when injected into male Swiss mice 10 min after training, as indicated by retention performance 48 h later. The amnestic effect of PTZ was prevented by naltrexone (0.01 or 0.10 mg/kg, ip) administered after training, but prior to PTZ-treatment. On the contrary, neither naltrexone methyl bromide (0.01, 0.10, or 10.0 mg/kg, ip), a quaternarium analog of naltrexone, nor MR2266 (0.01 or 0.10 mg/kg, ip), a putative kappa opiate receptor antagonist, modified the behavioral effects of PTZ. On the other hand, the body seizures produced by PTZ were unaffected by any of the three opiate receptor antagonists that were given before the convulsant. Taken together, these results suggest that the effects of PTZ on retention are mediated, at least in part, by opioid peptides of central origin, and rules out a possible participation of opioid peptides derived from prodynorphin-precursor molecule. Administration of beta-endorphin (0.01 or 0.10 microgram/kg, ip) 10 min prior to testing attenuate the retrograde amnesia caused by PTZ. The effect of beta-endorphin was prevented by the simultaneous administration of naltrexone (0.10 mg/kg, ip) prior to testing. Naltrexone has no effect of its own upon retrieval. These results suggest that the impairment of retention induced by PTZ is probably due, at least in part, to a release of opioid peptides in the brain during the post-training period. PTZ given after training do not affect consolidation or memory storage, as mice thus treated may retrieve the learned information when they are submitted to an appropriate neurohumoral and/or hormonal state in the test session, that is, beta-endorphin injection. Therefore, the action of PTZ would be primarily at the level of the mechanism that make stored information available for late retrieval.
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PMID:The impairment of retention induced by pentylenetetrazol in mice may be mediated by a release of opioid peptides in the brain. 282 89

Immediate post-training administration of the central acting opioid receptor antagonist naltrexone (0.01-1.00 mg/kg) facilitated 48-h retention of a one-trial inhibitory avoidance task. An inverted-U dose-response curve was obtained. In this dose range naltrexone did not significantly affect response latencies of mice not given a footshock during the training. However, higher doses of naltrexone (3.0 and 10.0 mg/kg) increased latencies of both shocked and unshocked mice. The peripheral-acting opioid receptor blocker, naltrexone methyl bromide (MR 2263) (0.01-10.00 mg/kg), did not significantly influence retention latencies of either shocked or unshocked mice. Further, MR 2263 (0.1, 1.0, or 10.0 mg/kg) did not block the retention impairment produced by concurrently administered morphine (3.0 mg/kg) or beta-endorphin (0.1 microgram/kg). These findings indicate that the effect of these agonists on memory are not due to a peripheral influence. However, MR 2263 does prevent the memory-impairing effect of both metenkephalin (1.0 microgram/kg) and leu-enkephalin (0.3 microgram/kg) on retention. Those results suggest that enkephalins affect retention through influences initiated peripherally. Thus, different sites and mechanisms of action for beta-endorphin and the enkephalins are proposed.
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PMID:Pharmacological evidence of a central effect of naltrexone, morphine, and beta-endorphin and a peripheral effect of met- and leu-enkephalin on retention of an inhibitory response in mice. 293 40

The role of the second messengers cAMP and Ca++ in the control of proopiomelanocortin (POMC) gene expression was investigated with the use of hybridization with cloned complementary DNA probes. The effects of cAMP-related drugs on POMC messenger RNA (mRNA) levels were assessed in primary cultures of intermediate (IL) and anterior rat pituitary cells maintained in serum-free medium. 8-Bromo-cAMP (1 mM), but not 8-bromo-cGMP (1 mM), induced a 2-fold increase in IL and anterior lobe cell after 2 days of treatment. A similar increase was obtained with the adenylate cyclase-activating drugs forskolin (1 microM) and cholera toxin (100 ng/ml) or the phosphodiesterase inhibitor RO 20-1724 (100 microM). At 48 h, all these treatments had increased beta-endorphin accumulation in the medium and transiently decreased the cellular beta-endorphin content in IL cells, suggesting a parallel effect of cAMP-related drugs on secretion and biosynthesis. Incubating the cells with the Ca++ channel antagonists D600 (50 microM), verapamil (50 microM), and the dihydropyridine nifedipine (0.1 microM) decreased basal POMC mRNA levels, whereas the dihydropyridine BAYK 8644 (0.1 microM), which activates the Ca++ channel, increased POMC mRNA levels after 2 days. In addition, nifedipine decreased the stimulatory effect of forskolin, whereas BAYK 8644 further stimulated the forskolin-increased POMC mRNA levels in IL cells. We conclude that both Ca++ and cAMP may regulate the gene expression of POMC.
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PMID:Calcium ion and cyclic adenosine 3',5'-monophosphate regulate proopiomelanocortin messenger ribonucleic acid levels in rat intermediate and anterior pituitary lobes. 302 21

It is known that opioids stimulate prolactin (PRL) secretion by an action on hypothalamic neurons, but in vitro studies have suggested a direct action on the lactotrophs. The present study was performed on male rats known to have little or no PRL response to TRH. A beta-endorphin (beta EP) injection in the third ventricle stimulated PRL secretion and induced furthermore a PRL secretory reaction to TRH injected intravenously 20 min later. Pretreatment with naloxone 10 min before beta EP injection abolished not only the PRL response to beta EP but also the conjugated effect of beta EP and TRH. Pretreatment with naloxone methyl bromide (Br-naloxone), a quaternary naloxone derivative, which does not cross the blood-brain barrier, had no effect on the PRL response to beta EP but prevented the conjugated effect of beta EP and TRH on PRL secretion. Pretreatment of the animals with -methyl-parathyrosine resulting in a dopamine depletion or with haloperidol, a dopamine antagonist, could not induce lactotroph responsiveness to TRH. These results suggest that beta EP in male rat sensitizes the PRL cell to TRH by a direct effect and not through an inhibition of the dopaminergic tone.
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PMID:Opioid modulation of thyrotropin releasing hormone induced prolactin secretion. 310 8

The effects of morphine HCl and a synthetic met-enkephalin analogue [D-Ala2,MePhe4,Met(O)5ol]enkephalin (FK 33-824) on gastric damage produced by the intraperitoneal administration of indomethacin (10 mg/kg i.p.) have been investigated. Rats intraperitoneally pretreated with morphine HCl (10 mg/kg i.p.) and FK 33-824 (1 mg/kg i.p.) showed a statistically significant reduction both of the number and intensity of lesions induced by indomethacin. This protection was reversed by naloxone HCl (2 mg/kg i.p.). The protective effect was not related to a reduction of gastric secretion since the antisecretory drug cimetidine (25 mg/kg i.p.) and methscopolamine bromide (10 mg/kg i.p.) did not significantly prevent mucosal damage under the same experimental conditions.
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PMID:Effects of morphine and met-enkephalin analogue on gastric lesions induced by indomethacin. 360 43

Serial semithin sections of rat neurohypophysis were immunostained with 2 antibodies to enkephalins using the peroxidase antiperoxidase method. One of the antibodies (R133) recognizes both met- and leu-enkephalin whereas the other (R26) reacts with met-enkephalin only. After cyanogen bromide pretreatment of the sections the antibody R133 stained only a subpopulation of nerve endings that were distinct from those stained with the latter antibody. R26-(met-enkephalin-like) immunoreactivity was totally abolished by cyanogen bromide pretreatment. This preincubation method which selectively interferes with the staining of met-enkephalin terminals may help to discriminate the two enkephalins in immunocytochemical preparations.
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PMID:Cyanogen bromide cleavage of methionine residues as a control method for enkephalin immunocytochemistry. 390 10

The 41-residue sequence of recently identified ovine corticotropin-releasing factor (CRF) was assembled on a benzhydrylamine resin support. Deprotection and cleavage from the resin were accomplished by HF treatment. The crude peptide was purified by gel filtration and reverse-phase, medium pressure, followed by high-performance liquid chromatography (HPLC). In addition to the usual criteria, the homogeneity of the final material, obtained in 7% yield, was assessed by the isolation and examination of cyanogen bromide cleavage and tryptic digestion fragments by HPLC and amino acid analysis. The synthetic 41 amino acid CRF stimulated the release of corticotropin (ACTH) in three in vitro systems: isolated rat pituitary quarters, monolayer cultures of dispersed pituitary cells, and superfused pituitary cells on a column, the responses being related to the log-dose of CRF in the range of 0.05-125 ng/ml. The synthetic peptide also augmented in vivo release of ACTH in rats pretreated with chlorpromazine, morphine, and Nembutal, as assessed by the measurement of serum corticosterone. The data indicates chemical purity and high biological activity of synthetic material.
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PMID:Synthesis and biological properties of ovine corticotropin-releasing factor (CRF). 629 Aug 14

Acid extracts of human pancreas and gastric corpus and antral mucosa and muscularis were investigated for the presence of met-enkephalin and leu-enkephalin by radioimmunoassay, Sephadex chromatography and radioreceptor assay. As the assays for leu-enkephalin crossreacted with those for met-enkephalin, only cyanogen bromide-treated samples were used for the determination of leu enkephalin. Met-enkephalin immunoreactivity was destroyed by more than 94% when treated with cyanogen bromide. Serial extract dilutions displaced 125 I labelled met-enkephalin and 125 I leu-enkephalin in the respective enkephalin radioimmunoassay both roughly parallel to the standard curves. Sephadex chromatography of the extracts resulted in elution of met-enkephalin and leu-enkephalin immunoreactivity similar to the size of 3H-met-enkephalin, and these eluates displaced 3H-met-enkephalin from rat brain membranes in an opioid radioreceptor assay. The highest concentration of met-enkephalin and leu-enkephalin immunoreactivity in tissue obtained at surgery was in the mucosa of the body of the stomach. Met- and leu-enkephalin receptor bioreactivity concentrations exceeded immunoreactivity concentrations. These investigations provide evidence of the presence of met-enkephalin- and leu-enkephalin-like substances in human stomach and pancreas.
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PMID:Met- and leu-enkephalin immuno- and bio-reactivity in human stomach and pancreas. 716 59


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