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 opioid peptides on a 1.1-kb long proopiomelanocortin messenger RNA (POMC mRNA) have been investigated in rat hypothalamic cells maintained in culture. Most opioid peptides exerted an inhibitory control on POMC mRNA steady-state concentrations. beta-Endorphin caused a 65% maximal inhibitory effect (IC50 = 6.1 x 10(-9) M) while slightly less inhibition was caused by Met- and Leu-enkephalin, dynorphin A and DADLE ([D-Ala2,D-Leu5] enkephalin). The effects of beta-endorphin and of Met-enkephalin were completely reversed by the delta opioid antagonist ICI 174,864 while the kappa-receptor specific antagonist binaltorphimine or the sigma-receptor specific antagonist DTG (1,3-di(2-tolyl) guanidine) respectively blocked the inhibitory actions of dynorphin A and of DADLE. The mu-receptor specific agonist DAGO ([D-Ala2,N-Me-Phe4,Gly5-OL]enkephalin) did not affect POMC mRNA levels. The failure of the dopaminergic D2 antagonist haloperidol to modify the inhibitory effects of opioid peptides argues for a direct inhibitory opioid peptide modulation of hypothalamic POMC mRNA levels mediated by the delta-, kappa- and sigma- (but not mu-) receptors in vivo.
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PMID:Regulation of proopiomelanocortin messenger RNA concentrations by opioid peptides in primary cell cultures of rat hypothalamus. 164 65

The binding and internalization of a novel adrenocorticotropic hormone (ACTH) analog having a potent neuromodulating effect, ebiratide (H-Met(O2)-Glu-His-Phe-D-Lys-Phe-NH(CH2)8NH2), by isolated bovine brain capillaries, were examined. Metabolism of [5-125I-His]ebiratide occurred during a 30-min incubation with bovine brain capillaries at 37 degrees C. In the presence of 20 mM EDTA, added to inhibit this metabolism, the medium, after 30 min of incubation, contained 82.3 +/- 0.5% of the unchanged ebiratide. The total binding and acid-resistant binding of [125I]ebiratide increased with time and reached an equilibrium at about 15 min. The total binding and acid-resistant binding at 30 min (as the cell/medium ratios corrected with [14C]sucrose) were 13.07 +/- 0.86 and 5.00 +/- 0.18 microliters/mg of protein, respectively. The acid-resistant binding showed significant dependence on temperature and medium osmolarity. The [125I]ebiratide binding was significantly inhibited by dansylcadaverine, an endocytosis inhibitor. The saturable acid-resistant binding was obtained by the addition of unlabeled ebiratide (100 nM-5 mM), and the maximal internalization capacity (Bmax) at 30 min was 144.2 pmol/mg of protein, with the half-saturation constant (KD) of 62.1 microM. The nonsaturable acid-resistant binding [cell/medium ratio in the presence of the unlabeled compound (1 mM or more)] was 2.2 microliters/mg of protein. The acid-resistant binding was significantly inhibited by human ACTH, poly-L-lysine, protamine and E-2078, a basic peptide, but was not inhibited by poly-L-glutamate, insulin or transferrin. These results demonstrate that ebiratide is transported through the blood-brain barrier via a basic peptide-specific absorptive-mediated endocytosis.
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PMID:Transport mechanism of a new behaviorally highly potent adrenocorticotropic hormone (ACTH) analog, ebiratide, through the blood-brain barrier. 165 Aug 27

Adrenocorticotropic (ACTH) and melanocyte stimulating (MSH) hormones have been demonstrated in the same cells in the cephalic half of the pars distalis of the chicken pituitary glands in three ways: (I) immunohistochemistry, (II) radioimmunoassay (RIA) using both anti-human or porcine ACTH and synthetic alpha-MSH antibodies, and (III) isolation and purification, followed by the determination of amino acid compositions of both hormones. The contents of ACTH and alpha-MSH are estimated by RIA to be 1600 and 10 ng/gland, respectively. ACTH missed 1 (des-Phe39-ACTH) or 2 residues (des-Glu38, Phe39-ACTH) from the C-terminal portion was also isolated. The recoveries of these ACTHs are differed from preparation to preparation. The complete amino acid sequence of chicken ACTH (39 residues) has been determined as NH2-Ser-Tyr-Ser-Met-Glu-His-Phe-Arg-Trp-Gly-Lys-Pro-Val-Gly-Arg-Lys-Arg- Arg- Pro-Ile-Lys-Val-Tyr-Pro-Asn-Gly-Val-Asp-Glu-Glu-Ser-Ala-Glu-Ser-Tyr-Pro- Met-Glu-Phe-OH Strikingly the amino acid sequence of chicken ACTH shows a closer resemblance to that from an amphibian, Xenopus (3 residue substitution) than that from another bird, the ostrich (7 residue substitution) or the turkey (at least 9 residue substitution).
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PMID:Characterization of chicken ACTH and alpha-MSH: the primary sequence of chicken ACTH is more similar to Xenopus ACTH than to other avian ACTH. 165 32

Intermediate pituitaries of the reptile, Anolis carolinensis, were separately pulse labeled with [3H]Trp and [3H]Tyr. The major form of alpha-MSH was purified by immunoprecipitation and isolated by reverse phase HPLC. Tryptic peptide analysis indicated that the [3H]Trp-labeled C-terminal fragment of Anolis alpha-MSH had the same retention time as mammalian ACTH(9-13) amide; however, the [3H]Tyr-labeled N-terminal fragment did not coelute with either mammalian ACTH(1-8) or N-acetyl-ACTH(1-8). Purification of alpha-MSH from 76 Anolis intermediate pituitaries confirmed that a sequence change had occurred in the N-terminal region of Anolis alpha-MSH. The tissues were acid extracted and purified by Sephadex G-25 chromatography and reverse phase HPLC to yield 4.5 micrograms of purified Anolis alpha-MSH for amino acid composition analysis and automated Edman degradation sequence analysis. The major form of Anolis alpha-MSH is nonacetylated and has the following novel primary sequence: Ser-Tyr-Ala-Met-Glu-His-Phe-Arg-Trp-Gly-Lys-Pro(Val-amide). The presence of Val-amide was verified by immunological analysis, tryptic peptide analysis and amino acid composition analysis.
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PMID:Detection of a novel sequence change in the major form of alpha-MSH isolated from the intermediate pituitary of the reptile, Anolis carolinensis. 166 89

The fasting plasma levels of corticotropin-releasing hormone (CRH), delta sleep-inducing peptide (DSIP), beta-endorphin (beta-END), methionine-enkephalin (m-ENK), beta-lipotropin (beta-LPH), and alpha-melanocyte-stimulating hormone (alpha-MSH) were measured by radioimmunoassay in 22 stable patients with chronic renal failure on regular hemodialysis treatment and compared with those of 10 healthy controls. The plasma concentrations of DSIP, beta-END, m-ENK, beta-LPH, and alpha-MSH were increased. The plasma level of CRH was not different from that of the controls. The elevated plasma levels of endogenous opioid peptides and DSIP may contribute to the uremic syndrome, although this must be further elucidated.
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PMID:Elevated plasma levels of opioid peptides and delta sleep-inducing peptide but not of corticotropin-releasing hormone in patients receiving chronic hemodialysis. 166 74

This study was designed to determine if opioids were detectable in cerebrospinal fluid (CSF) and if these concentrations were altered by hemorrhagic hypotension. This study was further designed to determine the effects of topically administered opioids on pial arteriolar diameter during normotension and hypotension. Closed cranial windows were used to determine pial arteriolar diameter. Periarachnoid cortical and cisterna magna CSF was collected from piglets during normotension and hypotension (systemic arterial pressure decreased from 63 +/- 1 to 33 +/- 1 mm Hg). Opioid profiles were assessed qualitatively by radioreceptor assay, and individual opioids were measured quantitatively by radioimmunoassay. Periarachnoid cortical and cisterna magna CSF methionine enkephalin-, leucine enkephalin-, dynorphin-, and beta-endorphin-like receptor active values all were increased by hypotension. When quantified by radioimmunoassay, periarachnoid cortical CSF values for methionine enkephalin-like immunoreactivity were 1,167 +/- 58 and 2,975 +/- 139 pg/ml for normotension and hypotension, respectively. Periarachnoid cortical CSF radioimmunoassay values for dynorphin-like immunoreactivity were 15 +/- 2 and 28 +/- 2 pg/ml for normotension and hypotension, respectively. When applied topically to the cortical surface, synthetic methionine enkephalin increased pial arteriolar diameter (134 +/- 4, 158 +/- 4, and 163 +/- 4 microns for control, 574 pg/ml [10(-10) M], and 5,740 pg/ml [10(-9) M], respectively). Similarly, topical synthetic leucine enkephalin and dynorphin elicited pial arteriolar dilation. However, beta-endorphin produced arteriolar constriction. Hypotension attenuated methionine and leucine enkephalin-induced dilation and reversed dynorphin-induced dilation to concentration-dependent constriction. beta-Endorphin-induced constriction was not changed by hypotension. Therefore, opioids could contribute to the control of the cerebral circulation during hypotension.
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PMID:Opioids in cerebrospinal fluid in hypotensive newborn pigs. 167 30

Basal alkaline secretion of the denervated rat ileum was monitored by a pH-stat method. Changes of transepithelial electrical potential difference (PD) were also continuously registered. In other experiments net fluid transport was measured with a gravimetric method. The importance of the enteric nervous system for the recorded variables was investigated by giving i.v. hexamethonium, neuropeptide Y (NPY) or methionine-enkephalin or by stimulating electrically the mesenteric nerves surrounding the superior mesenteric artery. Alkaline secretion was inhibited by about 20% by mesenteric nerve stimulation or by neuropeptide Y (NPY) or met-enkephalin i.v. A somewhat greater inhibition (approximately 30%) of transepithelial electrical potential difference was elicited by the mesenteric nerve stimulation and NPY whereas met-enkephalin did not cause any transepithelial electrical potential difference change. Net fluid absorption was markedly diminished (by approximately 65-75%) by met-enkephalin but not by NPY. The cellular mechanisms underlying alkaline secretion were investigated by means of amiloride, SITS and acetazolamide. The basal alkaline secretion and transepithelial electrical potential difference were not influenced by 10(-3)M or 10(-4) SITS. In contrast 10(-3) M amiloride caused a significant increase of alkaline secretion but not of transepithelial electrical potential difference. A 35% reduction in the alkaline secretion but not transepithelial electrical potential difference was observed after acetazolamide had been given intravenously. A similar decrease was observed after giving hexamethonium. We conclude: (1) Enteric nerves are of comparatively small importance in controlling the ileal alkaline secretion recorded during basal conditions; (2) About 35% of the basal ileal alkaline secretion is carbonic anhydrase dependent. This mechanism is not influenced by nicotinic receptor blockade; (3) Under the present experimental conditions there may be an alkaline secretion which is concealed by a simultaneously operating Na+/H+ exchanger and; (4) No consistent quantitative correlation exists between alkaline secretion, transepithelial electrical potential difference and net field transport in the denervated rat ileum.
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PMID:On the mechanisms of the basal alkaline secretion in the rat ileum in vivo. 167 11

Recent experimental data indicate that endogenous brain ligands for the opioid receptors such as enkephalins, beta-endorphin (beta-End) and dynorphin (Dyn) may be involved in both generalized and partial seizures. The "tottering" (tg/tg) mouse provides an electrophysiological representation of generalized spontaneous human epilepsy. These mice exhibit behavioral absence seizures with accompanying spike-wave discharges. Methionine-enkephalin (M-Enk), beta-End and Dyn levels in various regions of brain were measured by radioimmunoassay (RIA) in 15-18-week-old tg/tg and control (+/+) mice to elucidate the relation between seizures and the opioid system. beta-End and Dyn levels were similar in tg/tg and +/+ mice. However, M-Enk levels were significantly increased in the striatum, cortex, pons and medulla of the tg/tg mice. Our data suggest that in the tottering mouse model of generalized epilepsy there is an alteration of enkephalinergic pathways and not of the endorphinergic or dynorphinergic pathways.
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PMID:Increased methionine-enkephalin levels in genetically epileptic (tg/tg) mice. 168 15

The present experiments were performed to determine whether the age-related loss of striatal D2 receptors could be localized to a kainic acid-sensitive neuronal population. This neurotoxin selectively destroys intrinsic neurons. Thus, if kainic acid reduced striatal D2 receptor concentrations such that age differences in this parameter were no longer observed, it would be a good indication that the D2 receptors lost through aging are also sensitive to kainic acid. Mature (6 months) and senescent (24 months) rats were stereotaxically, unilaterally injected with 3 micrograms/0.5 microliter kainic acid into the right striatum. Seven days later striatal D2 receptors were assessed with [3H]-spiperone in one group of mature and senescent rats. A second group of mature and senescent unilaterally lesioned rats was anesthetized and perfused. Brains were dissected and processed for striatal cell counts using cresyl violet staining, tyrosine hydroxylase and met-enkephalin using immunocytochemistry, and acetylcholinesterase using histochemistry. Age-related differences in D2-receptor concentrations were observed in intact, but not lesioned, striata. Kainic acid was less effective in reducing D2-receptor concentrations in senescent animals, suggesting that some proportion of the receptors was already lost prior to lesioning. Kainic acid also reduced total neuronal numbers, as well as Met-Enk and AChE positive staining, to approximately the same extent in mature and senescent rats. No age differences were seen in any of the other parameters following kainic acid administration.
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PMID:The deleterious effects of aging and kainic acid may be selective for similar striatal neuronal populations. 168 53

The experiments examine the actions of morphine and opioid peptides on the responses evoked by electrical field stimulation or by acetylcholine (ACh) and substance P (SP) in guinea-pig bronchial strip chain. Electrical field stimulation evoked a biphasic contraction, consisting of a cholinergically mediated fast contraction followed by a non-cholinergically mediated slow contraction. Morphine and opioid peptides caused a concentration-dependent inhibition in the height of the non-cholinergic contraction. The order of inhibitory activity was BW443C greater than dynorphin greater than morphine greater than beta-endorphin greater than leucine-enkephalin greater than methionine-enkephalin. Cholinergically mediated contractions were less potently inhibited by these opioids. Submaximal contractions of bronchial muscle evoked by exogenous ACh (2 microM) or SP (0.2 microM) were not inhibited by morphine (100 microM) or opioid peptides (3-10 microM), rather, they were augmented. The results indicate that in guinea-pig isolated bronchial muscle, morphine and opioid peptides can selectively inhibit excitatory non-cholinergic neurotransmission via prejunctional opioid receptors.
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PMID:Morphine and opioid peptides selectively inhibit the non-cholinergically mediated neurogenic contraction of guinea-pig isolated bronchial muscle. 169 28


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