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)

Acute ethanol treatment in vivo (i.p. injection of 3.5 g ethanol/Kg B. wt.) stimulated the release of beta-endorphin like peptides by the pituitary gland as was indicated by the increased content of beta-endorphin like immunoreactivity (beta-EPLIR) in the plasma. Furthermore, a significant decrease in the anterior lobe content of beta-EPLIR was observed, while the decrease in the neurointermediate lobe beta-EPLIR content at 45 min after the i.p. ethanol injection was not statistically significant. In vitro incubation of neurointermediate lobes, from animals injected with either ethanol or saline, in the presence of 3H phenylalanine indicated that the content of beta-EPLIR in the incubation medium was increased, the content of the newly biosynthesized 3H-phenylalanine labelled proteins in the neurointermediate lobe extract was decreased, while the content of 3H-phenylalanine labelled pro-opiomelanocortin, beta-lipotropin and beta-endorphin in the neurointermediate lobes extract were not significantly changed by the ethanol treatment, though a small increase was observed. When neurointermediate lobes from untreated control animals were incubated for 3 hrs with 3H-phenylalanine in the presence or absence of 300 mg ethanol per 100 ml incubation medium, there was no significant difference in the beta-EPLIR content in the incubation medium, or in the content of 3H-phenylalanine labelled proteins, pro-opiomelanocortin, beta-lipotropin and beta-endorphin in the neurointermediate lobe extract. These results suggest that ethanol has little or no direct effect on the beta-endorphin peptides in the pars intermedia cells.
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PMID:Effect of acute ethanol in vivo and in vitro on the beta-endorphin system in the rat. 294 90

The immunohistochemical distribution of opioid peptides derived from proenkephalin A in the rat pituitary was studied by indirect immunofluorescence; immunoreactive peptides were also characterized by column chromatography followed by specific RIAs. Nerve terminals in the neural lobe were immunoreactive (ir) for Tyr-Gly-Gly-Phe-Met-Arg-Phe (YGGFMRF), Tyr-Gly-Gly-Phe-Met-Arg-Gly-Leu (YGGFMRGL), and met-enkephalin [Tyr-Gly-Gly-Phe-Met (YGGFM)]. All cells in the intermediate lobe were ir for YGGFMRF, while only occasional cells exhibited YGGFMRGL-like immunoreactivity, and YGGFM-ir cells were not detected in this lobe. In the anterior lobe, some large ovoid cells, identified as gonadotrophs, were immunoreactive for enkephalins. The number of YGGFMRF-ir cells was larger than the number of YGGFMRGL- and YGGFM-ir cells, and these opioid peptides were present in cells that did not contain beta-endorphin immunoreactivity. Twenty times more YGGFMRF than YGGFMRGL-immunoreactivity was present in the anterior lobe, whereas the neurointermediate lobe obtained 4 times more ir YGGFMRF than YGGFMRGL. Pituitary lobe extracts contained substantial amounts of high mol wt forms of ir YGGFMRF and YGGFMRGL, but not of YGGFM or Leu-enkephalin (Tyr-Gly-Gly-Phe-Leu). Low mol wt ir peptides present in both lobes consisted largely of the authentic peptides when analyzed by HPLC; however, an unidentified YGGFMRF-ir peptide was also detected. The results indicate that the proenkephalin A molecule may be processed differentially in the various compartments of the pituitary gland and that opioid peptides derived from this precursor may have functional roles in all three lobes. The relatively large amount of YGGFMRF immunoreactivity, which was detected both biochemically and immunohistochemically, indicates that YGGFMRF-ir peptides may be important proenkephalin A-derived products in the pituitary gland.
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PMID:Enkephalins in the rat pituitary gland: immunohistochemical and biochemical observations. 295 13

The effect of soman poisoning on the levels of methionine enkephalin and beta-endorphin in mice and rats were determined. Soman poisoning produced no significant effect on methionine enkephalin levels in the striatum of rats or mice or beta-endorphin levels in the pituitary gland of mice. In rats beta-endorphin levels were significantly reduced 24 hr post soman poisoning, but returned to control levels by 48 hr. In vitro, the hydrolysis of leucine enkephalin by aminopeptidase was virtually complete by 30 min and found to be the major route of degradation. The release of TYR-GLY-GLY in the presence or absence of puromycin (10 microM) was found to be low (less than or equal to 2.0%). A minor effect on TYR release in the presence of GLY-GLY-PHE-MET (50 microM) was insignificant. Preincubation of mouse striatum homogenates with soman (1 or 10 microM) did not inhibit the hydrolysis of leucine enkephalin. These results suggest that the long term antinociception following soman exposure is not due to either altered concentration of endogenous opioid-like substances or inhibition of the enzymes responsible for their degradation.
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PMID:Role of endogenous opioids in soman (pinacolyl methylphosphonofluoridate)-induced antinociception. 295 88

Male Sprague Dawley rats were chronically pair-fed with liquid diets containing 6.5% (vol/vol) ethanol, or equicaloric sucrose. After 21 days the ethanol-containing diet was discontinued and both groups were fed the sucrose diet. Groups of animals were killed on day 22 (0 day of ethanol withdrawal) and 1, 3, 8, and 15 days after ethanol withdrawal and the neurointermediate lobes (NILs) were removed and incubated with [3H]phenylalanine for 3 h. Chronic ethanol treatment induced an increase in the biosynthesis and release of beta-endorphin-like peptides by the rat NIL. After ethanol withdrawal the beta-endorphin-like immunoreactivity content in the NIL and the in vitro release of immunoreactive beta-endorphin (beta EP) by the NIL were significantly lower than in the controls on the first day, whereas no significant difference was found on days 3, 8, and 15 after ethanol withdrawal. The in vitro incorporation of [3H]phenylalanine into POMC, beta-lipotropin and beta EP was found to be higher in the ethanol-treated animals than in the controls on days 0, 1, and 3 after ethanol withdrawal, with no significant difference on days 8 and 15 after ethanol withdrawal. Furthermore, in both the ethanol-treated animals and their pair-fed controls the rate of incorporation of [3H]phenylalanine into total proteins, POMC, beta-lipotropin, and beta EP was significantly higher on days 8 and 15 after ethanol withdrawal than on the day of ethanol withdrawal (day 0), suggesting the implication of a nutritional factor. HPLC analysis of the beta EP peptides indicated that the percentage of acetylated forms of beta EP was higher in the NIL of the alcohol-treated animals, especially on days 8 and 15 after ethanol withdrawal. This observation suggests that though the rates of biosynthesis and release of beta EP-related peptides have returned to normal at 15 days after ethanol treatment, the activity of the enzyme responsible for the acetylation of beta EP remained elevated.
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PMID:Effects of ethanol treatment and withdrawal on biosynthesis and processing of proopiomelanocortin by the rat neurointermediate lobe. 296 39

The effect of synthetic atriopeptins on basal and stimulated aldosterone secretion was determined in isolated adrenal glomerulosa cells of the rat. Neither atriopeptin I (1-21) or III (1-24, i.e., the Phe-Arg-Tyr carboxy-terminal extension of atriopeptin I) altered basal aldosterone release. However, if the cells were prepared from adrenals of sodium-depleted rats, the basal aldosterone release was increased by 9-fold, compared with cells from normal rats. This elevated release was inhibited by 32% by atriopeptin I and atriopeptin III. Atriopeptin III was more potent than atriopeptin I. Angiotensin II and adrenocorticotropin stimulated the release of aldosterone in a concentration-related manner. Both atriopeptin I and atriopeptin III inhibited the stimulation by the peptides. Atriopeptin I inhibited angiotensin II- and adrenocorticotropin-induced aldosterone production by 50% at concentrations of 12 and 11 nM, respectively, and 0.5 and 0.2 nM, respectively, for atriopeptin III. Potassium-stimulated aldosterone production was also inhibited by atriopeptin I and atriopeptin III with 50% inhibition at concentrations of 10 and 0.4 nM, respectively. Shorter peptides (1-20, 1-19, and 3-19) were equipotent to atriopeptin I (1-21) as inhibitors of angiotensin II-induced steroidogenesis. To determine the site at which atriopeptins inhibit aldosterone synthesis, we used cyanoketone to inhibit 3 beta-hydroxy-dehydrogenase and dissociate the early and late pathways. Angiotensin II (2 nM) increased the synthesis of pregnenolone (early pathway), as well as the conversion of [3H]corticosterone to [3H]aldosterone (late pathway). Atriopeptin III inhibited basal pregnenolone synthesis by 36% and completely blocked angiotensin II-stimulated synthesis. The peptide similarly inhibited the late pathway.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of aldosterone biosynthesis by atriopeptins in rat adrenal cells. 298 17

The fluorescein-labeled melanotropin [N alpha-chlorotriazinylaminofluorescein-Ser1,Nle4,D-Phe 7]-alpha-MSH, was prepared by solid-phase techniques of peptide synthesis. The biological actions of this analogue were determined in several melanocyte bioassays and were compared with the parent peptide [Nle4,D-Phe7]-alpha-MSH and the native hormone alpha-MSH. The fluorescein compound was a superpotent agonist with approximately 10 times more activity than alpha-MSH in both the frog and the lizard skin bioassays. Murine S91 melanoma cells assayed in vitro (tyrosinase bioassay) were as responsive to the fluorescein analogue as to alpha-MSH. The analogue exhibited ultraprolonged biological activity and the biological activities were unaffected by treatment of the analogue with alpha-chymotrypsin. The fluorescein-labeled melanotropin should prove useful for melanotropin receptor characterization.
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PMID:Synthesis and biological evaluation of the superagonist [N alpha-chlorotriazinylaminofluorescein-Ser1,Nle4,D-Phe7]-al pha-MSH. 298 82

The conversion of BAM-12P to Met-enkephalin and the hydrolysis of the Phe-Met and Phe-Leu bonds of met-enkephalin-Arg-Phe and Leu-enkephalin-Arg-Arg, respectively, by rabbit brain endo-oligopeptidase A were demonstrated. Peptide fragments were isolated by high performance liquid chromatography and identified by amino acid analysis. BAM 22P was not hydrolysed by the enzyme. The concentration dependent inhibition of BAM-12P conversion into Met-enkephalin by bradykinin and vice-versa provided additional evidence that endo-oligopeptidase A cleaves both the Phe5-Ser6 bond in bradykinin and the Met5-Arg6 bond of BAM-12P.
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PMID:Conversion and inactivation of opioid peptides by rabbit brain endo-oligopeptidase A. 299 91

The in vivo effects of a number of opioid agonists and antagonists were studied on the spontaneous reflex contractions of the urinary bladder recorded isometrically in the rat anesthetized with urethane. All substances were administered into the central nervous system by the intracereboventricular (i.c.v.) or spinal intrathecal (i.t.) route. The conformationally restricted enkephalin analogues [2-D-penicillamine, 5-L-cysteine] enkephalin (DPLCE), [2-D-penicillamine, 5-L-penicillamine] enkephalin (DPLPE) and [2-D-penicillamine, 5-D-penicillamine] enkephalin (DPDPE) produced dose-related inhibition of reflex bladder contractions when administered by the i.c.v. or i.t. route. Both the novel delta-opioid receptor antagonist ICI 154,129 (200-600 micrograms) [N,N-bisallyl-Tyr-Gly-Gly-Psi-(CH2S)-Phe-Leu-OH) and ICI 174,864 (1-3 micrograms) [N,N-dially-Tyr-Aib-Aib-Phe-Leu-OH: Aib = alpha-aminoisobutyric acid] attenuated or abolished the effects of DPLCE, DPLPE and DPDPE when administered by the i.c.v. or i.t. route. The antagonism observed was selective since the equipotent inhibition produced by the mu-opioid receptor agonist [D-Ala2, Me-Phe4, Gly(ol)5] enkephalin (DAGO) was unaffected. Overall, ICI 154,129 was considerably weaker than ICI 174,864 and both antagonists inhibited bladder activity at doses higher than those required to demonstrate delta-receptor antagonism. Further studies of the agonistic effect of ICI 174,864 showed that it was insensitive to low doses of naloxone (2 micrograms, i.c.v. or i.t.) but could be abolished by higher (10-15 micrograms) doses of naloxone. These observations suggested that the agonistic effect of ICI 174,864 was not mediated by mu-opioid receptor. beta-Endorphin (0.2-1.0 micrograms, i.c.v.) inhibited bladder contractions but following recovery from this effect, appeared to prevent the expression of delta-receptor antagonism by ICI 174,864. In addition a previously subthreshold dose of ICI 174,864 now exhibited marked agonistic activity. The inhibitory effect of a submaximal dose of DPDPE was also potentiated by beta-endorphin under these circumstances. These observations suggest that supra-spinal and spinal delta-opioid receptors are involved in the opioid-mediated inhibition of reflex bladder contractions in the rat. Moreover beta-endorphin may be important in regulating central delta-opioid receptors.
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PMID:Central delta-opioid receptor interactions and the inhibition of reflex urinary bladder contractions in the rat. 299 71

The aim of this study was to investigate further the influence of dermorphin (D), a new potent opioid peptide (H-Tyr-D-Ala-Phe-Gly-Tyr-Pro-Ser-NH2), on the functional activity of the pituitary-adrenocortical system in man. Six normal men were treated with oral metyrapone to stimulate the secretion of ACTH, beta-lipotropin, and beta-endorphin. In these subjects, significant suppression of metyrapone-evoked release of ACTH and related peptides occurred during D infusion (5.5 micrograms/kg X min for 30 min) compared with that during saline infusion. These results indicate that D can induce a significant decline in plasma levels of ACTH, beta-lipotropin, and beta-endorphin, the major circulating peptides from the C-terminal part of proopiocortin, and suggest that opioid peptides may be involved in the control of the functional activity of pituitary-adrenocortical activity in man.
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PMID:Dermorphin reduces the metyrapone-evoked release of adrenocorticotropin, beta-endorphin, and beta-lipotropin in man. 299 56

Spontaneous reflex bladder contractions were recorded isometrically in urethane anesthetized rats. Bladder contractions were depressed by intracerebroventricular injections of the mu-opioid receptor agonist [D-Ala2,MePhe4,Gly(ol)5]enkephalin (DAGO) and the delta-agonist [2D-penicillamine,5D-penicillamine]enkephalin (DPDPE) respectively. The effect of DPDPE was selectively antagonized by ICI 174,864 (N,N-diallyl-Tyr-Aib-Aib-Phe-Leu-OH; Aib = alpha-aminoisobutyric acid). However following the administration of beta-endorphin the antagonistic action of ICI 174,864 could no longer be observed. In addition ICI 174,864 exhibited agonistic activity following beta-endorphin and the effects of DPDPE were prolonged in a dose related manner by beta-endorphin. These observations suggest that beta-endorphin may produce complex changes in central delta-opioid receptor activity.
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PMID:Centrally administered beta-endorphin produces prolonged changes in delta-opioid ligand activity in vivo. 300 7


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