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)

Rabbits were anesthetized with urethane and were given intracisternal injections of the following substances: adrenocorticotropin, beta-melanocyte stimulating hormone, choroid plexus peptide IIF, epinephrine, serotonin, histamine, oxytocin, lysine and a arginine vasopressins, acetylcholine and melatonin. The effects on the concentration of 3', 5' cyclic guanosine monophosphate (cGMP) in cerebrospinal fluid were then measured. Only melatonin and acetylcholine caused a significant (p less than 0.05) effect on cGMP concentration. Both agents increased the nucleotide's concentration within 30 min. Melatonin was about 1,000 times more potent than acetylcholine; the mininal effective doses were 1 mug and 1,000 mug, respectively.
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PMID:Injection of melatonin into cisterna magna increases concentration of 3', 5' cyclic guanosine monophosphate in cerebrospinal fluid. 18 65

Human peripheral lymphocytes were broken in a Dounce homogenizer and subcellular fractions enriched in plasma membranes or microsomal particles and mitochondria were isolated by centrifugation through a discontinuous sucrose gradient. Various agents that promote cyclic AMP accumulation in intact lymphocytes were compared in their ability to stimulate adenylate cyclase activity in the individual fractions. Plasma-membrane-rich fractions that were essentially free of other subcellular particles as judged by electron microscopy and marker enzyme measurements responded to fluoride, but weakly or not at all to prostaglandin E1 and other prostaglandins. Microsomal and mitochondrial-rich fractions responded markedly to both prostaglandin E1 and fluoride. In some, but not all, experiments phytohaemagglutinin produced a modest increase in enzyme activity in plasma-membrane-rich fractions. Catecholamines, histamine, parathyrin, glucagon and corticotropin produced little or no response. In the absence of theophylline, adenosine (1-10 micronM) stimulated basal enzyme activity, although at higher concentrations the responses to prostaglandin E1 and fluoride were inhibited. GTP (1-100 micronM) and GMP(5-1000 micronM) respectively inhibited or stimulated the response to fluoride, whereas the converse was true with prostaglandin E1.
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PMID:Adenylate cyclase activity in lymphocyte subcellular fractions. Characterization of non-nuclear adenylate cyclase. 19 77

Selective dispersion of melanosomes was often observed after iontophoretic injection of cyclic adenosine monophosphate (AMP) from a glass microelectrode positioned in a target melanophore in frog skin (as viewed from above through a microscope), with other melanophores in the field serving as controls. Because the skin has orderly arrays of several types of closely spaced cells, it is probable that at times the microelectrode also impales cells other than melanophores. When cyclic AMP injection inside a cell resulted in dispersion of melanosomes from a perinuclear position into dendritic processes, the onset of dispersion was relatively rapid, in many cases less than 4 min (mean time of onset, 5.3 +/- 2.9 [SD] min). A much slower dispersion (mean time of onset, 19.0 +/- 5.0 min) of melanosomes was observed when the microelectrode was positioned adjacent to a melanophore, and much larger quantities of cyclic AMP were released. In addition, no changes were observed for injections of 5'-AMP or cyclic guanosine monophosphate (GMP) through electrodes positioned inside or adjacent to melanophores. Potential measurements showed that after impaling a clell, a constant transmembrane potential could often be recorded over many minutes, indicating that the membrane tends to seal around the microelectrode. The results indicate that cyclic AMP acts more rapidly on the inside of a cell than when applied outside a cell and allowed to diffuse through the plasma membrane. This study introduces a model system whereby the properties of the plasma membrane and melanocyte-stimulating hormone (MSH) receptors can be studies within a single target cell.
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PMID:Iontophoretic release of cyclic AMP and dispersion of melanosomes within a single melanophore. 19 12

The effects of intravenous human atrial natriuretic factor ANF(99-126) administration on anterior pituitary hormone secretion have not been extensively investigated in humans. We repeatedly studied 10 healthy volunteers (5 female, 5 male, aged 28 +/- 2 years) on 2 occasions, 3 days apart. In randomized, single blind order, subjects received pretreatment with either placebo or intravenous ANF(99-126) (bolus 100 micrograms/kg, 30-min infusion of 0.1 micrograms/kg.min). Subsequently on both occasions subjects received a combined intravenous bolus injection of pituitary releasing hormones (200 micrograms thyrotropin releasing hormone, 100 micrograms gonadotropin releasing hormone and 100 micrograms human adrenocorticotropin releasing hormone; Bissendorf, Hannover, FRG). Plasma concentrations of adrenocorticotropic hormone (ACTH), cortisol, luteinizing hormone (LH), follicle-stimulating hormone (FSH), growth hormone (GH), thyrotropin (TSH), prolactin, ANF and cyclic guanosine monophosphate (GMP) were determined by radioimmunoassay. ANF(99-126) treatment induced a significant reduction in basal ACTH plasma concentrations and tended to decrease basal plasma cortisol. The TSH response to combined releasing hormone administration was significantly diminished after ANF(99-126) pretreatment. In women, the releasing hormone induced prolactin increase was reduced after ANF(99-126) pretreatment. With the present study design, ANF(99-126) did not alter the basal or releasing hormone stimulated plasma concentrations of cortisol, LH, FSH and GH. Releasing hormone administration did not affect ANF and cyclic GMP plasma levels. In humans, effects of natriuretic peptides on anterior pituitary hormone secretion may have to be considered with investigational or therapeutic administration of ANF analogues or agents interfering with the ANF metabolism.
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PMID:Effects of atrial natriuretic factor on anterior pituitary hormone secretion in normal man. 139 23

Some of the functional effects of beta-endorphin on immune cells are resistant to inhibition by naloxone. To further characterize the beta-[125I]endorphin-binding site mediating these effects and its response to cations and GTP, the human monocyte-like cell line U937 was used. Incubation of intact cells and beta-[125I]endorphin for 60 min at 4 C demonstrated a saturable, high affinity binding site [Kd = 1.2 +/- 0.5 X 10(-8) M (mean +/- SE; n = 4] competed by equimolar beta-endorphin and N-acetyl (Ac)-beta-endorphin but not by naloxone, morphine, or selective opiate receptor agonists. Competition studies showed that beta-endorphin-(6-31) and beta-endorphin-(28-31) were approximately 5- and 100-fold less potent, respectively, whereas beta-endorphin-(1-16) or -(1-27) was ineffective. Covalent cross-linking of beta-[125I]endorphin to intact cells and resolution by gel electrophoresis showed dominant bands at 59K and 44K and a minor band at 66K. The bands at 44K and 66K were completely displaced by increasing equivalent concentrations of beta-endorphin and N-Ac-beta-endorphin. Increasing concentrations of mono (Na+, K+)- and divalent (Ca2+, Mg2+, Mn2+) cations reduced the binding of beta-[125I]endorphin to U937 membrane; beta-[125I]endorphin binding to rat brain membrane showed similar cation sensitivity. GTP gamma-sulfate (GTP gamma S; 10(-4) M) alone reduced binding to U937 membrane by 25%. In the presence of Na+ (100 or 150 mM) or Mg2+ (10 mM), GTP gamma S reduced binding by an additional 50%. Moreover, GTP gamma S (10(-8)-10(-4) M) in the presence of Na+ (100 mM) reduced binding in a dose-dependent manner, whereas GMP was ineffective. In conclusion, beta-endorphin binds to sites on human U937 cells similar to those observed on normal murine splenocytes. Although naloxone insensitive, these sites exhibit properties, such as size, salt sensitivity, and coupling to a GTP-binding protein, that are similar to those observed for agonist binding to brain opiate receptors.
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PMID:Beta-endorphin binding to naloxone-insensitive sites on a human mononuclear cell line (U937): effects of cations and guanosine triphosphate. 216 44

The present study evaluated the possible effect and mechanism of action of interleukin-1 beta in regulating the release of corticotropin-releasing factor and adrenocorticotropin hormone from human cultured placental cells. With the use of a primary monolayer culture of human placental cells at term, the addition of interleukin-1 beta increased the release of immunoreactive corticotropin-releasing factor with a dose- and time-dependent effect. The intracellular concentration of both cyclic adenosine monophosphate and cyclic guanosine monophosphate increased in the presence of interleukin-1 beta. The addition of indomethacin, a prostaglandin synthesis inhibitor, partially reversed the effect of interleukin-1 beta. The same doses of interleukin-1 beta stimulated the release of adrenocorticotropin hormone and this effect was partially reversed by the addition of a synthetic corticotropin-releasing factor antagonist or by indomethacin. This study showed that interleukin-1 beta increases the release of corticotropin-releasing factor and adrenocorticotropin hormone from cultured placental cells. This effect is associated with increased intracellular cyclic nucleotide concentrations and is in part reversed by a prostaglandin synthesis inhibitor.
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PMID:Mechanism of action of interleukin-1 beta in increasing corticotropin-releasing factor and adrenocorticotropin hormone release from cultured human placental cells. 217 41

The authors examined the effect of topical application of agents known to increase cyclic nucleotide levels on tear secretion by accessory lacrimal gland tissue in their rabbit model for keratoconjunctivitis sicca (KCS). Tear secretion was studied by changes in tear film osmolarity and tear volume caused by application of the agents relative to application of isotonic buffer solution alone. A decrease in tear film osmolarity or increase in tear volume was interpreted as an increase in tear secretion. Irritative stimulation was distinguished from pharmacologic stimulation by the prior use of topical proparacaine. The following agents significantly decreased tear film osmolarity and increased tear volume: vasoactive intestinal peptide (2 X 10(-8) to 2 X 10(-6) M); three pro-opiomelanocortin fragments alpha-, beta-, and gamma-melanocyte stimulating hormone at 10(-4), 10(-3), and 10(-3) M, respectively; the permeable cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) analogs 8-Br cAMP (0.3-3.0 X 10(-3) M) and 8-Br cGMP (1.0-10.0 X 10(-3) M); and the cyclic nucleotide phosphodiesterase inhibitor 1-isobutyl-3-methyl xanthine (0.3-3.0 X 10(-3) M). Forskolin (2 X 10(-4) M), which activates the catalytic subunits of adenyl cyclase, increased tear volume significantly. Secretin, adrenocorticotropic hormone, and pilocarpine were ineffective. The authors conclude that agents that increase either cAMP or cGMP levels pharmacologically stimulated tear secretion when applied topically to rabbit eyes with surgically induced KCS.
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PMID:Stimulation of tear secretion by topical agents that increase cyclic nucleotide levels. 236 69

Adrenocorticotropic hormone (ACTH) inhibited replication in functional adrenal tumor cells with a concomitant stimulation of steroidogenesis and a characteristic change of morphology from a flattened to a spherical type. [(3)H]Thymidine incorporation into DNA was inhibited by about 50% 6 hours after ACTH treatment. Both cyclic AMP and dibutyryl cyclic AMP inhibited [(3)H]thymidine incorporation and caused the characteristic morphological change noted with ACTH. The extent of stimulation of steroidogenesis and the amount of inhibition of [(3)H]thymidine incorporation in response to various doses of ACTH were closely related and both were in parallel with the concentration of cyclic AMP in the cells. Cyclic GMP and cyclic IMP did not inhibit [(3)H]thymidine incorporation significantly, and did not change the morphology of the cells. AMP inhibited [(3)H]thymidine incorporation into DNA and caused the characteristic morphological change. However, AMP did not increase the cyclic AMP content of the cells. CMP, GMP, and UMP showed a significant inhibition of [(3)H]thymidine incorporation into DNA, but the extent of the inhibition was much less than that with AMP. These nucleotides did not change the morphology of the cells.
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PMID:Inhibition of replication in functional mouse adrenal tumor cells by adrenocorticotropic hormone mediated by adenosine 3':5'-cyclic monophosphate. 433 15

The inhibition of the calmodulin-mediated stimulation of bovine brain cyclic nucleotide phosphodiesterase activity (3':5'-cyclic adenosine monophosphate 5'-nucleotidohydrolase, EC 3.1.4.17) by the 31-residue opiate peptide beta-endorphin has been investigated. Using conditions in which porcine brain calmodulin (6 nM) is limiting (i.e., to give a 3-fold, Ca2+-dependent stimulation of enzymic activity toward cyclic guanosine monophosphate), the domain of beta-endorphin responsible for the inhibition was mapped by using a series of deletion peptides. beta-Endorphin exhibited an ED50 of several micromolar under the conditions employed, and several amino-terminal deletion peptides were essentially as inhibitory as the parent peptide. Methionine enkephalin and various carboxy-terminal deletion peptides had no demonstrable effect at concentrations of 100-200 microM. Peptides 1-25 and 1-27 (C' fragment) inhibited the calmodulin-dependent activity of phosphodiesterase, but higher concentrations were required than of beta-endorphin. Studies using combined amino- and carboxy-terminal deletion peptides demonstrate that peptide 14-25 was the shortest peptide examined that was capable of inhibiting calmodulin stimulation of phosphodiesterase activity under the conditions used. There was no evidence to indicate that the amino-terminal region comprising residues 1-13 of beta-endorphin contributes to the measured inhibition of calmodulin-stimulated enzymic activity. The circular dichroic spectra of calmodulin, beta-endorphin, and mixtures of the two were obtained, and the ellipticity of the peptide-protein mixtures at 221 nm exceeded that expected by assuming simple additivity. This finding is consistent with a direct interaction of beta-endorphin with calmodulin which seems to lead to enhanced helicity of one or both components.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Identification of beta-endorphin residues 14-25 as a region involved in the inhibition of calmodulin-stimulated phosphodiesterase activity. 631 22

Our study was designed to study the modulatory role of nitric oxide/cyclic guanosine monophosphate in the spinal cord on the antinociception induced by morphine and beta-endorphin given supraspinally. The antinociception was assessed by the tail-flick test in male ICR mice. The antinociception induced by intracerebroventricularly (i.c.v.) administered morphine was potentiated by intrathecal (i.t) injection of N omega-nitro-L-arginine (2 micrograms), hemoglobin (120 micrograms) or methylene blue (5 micrograms), but was attenuated by i.t. administered L-arginine (20 micrograms) or 3-morpholino-sydnonimine (SIN-1, 5 micrograms). In contrast, the antinociception induced by i.c.v. administered beta-endorphin was attenuated by i.t. pretreatment with N omega-nitro-L-arginine (2 micrograms) and the attenuation of beta-endorphin-induced antinociception by N omega-nitro-L-arginine was reversed by i.t. administered L-arginine (20 micrograms). The antinociception induced by i.c.v. administered beta-endorphin was also attenuated by i.t. administration of hemoglobin (120 micrograms) or methylene blue (5 micrograms). Intrathecal pretreatment with L-arginine did not affect i.c.v. administered beta-endorphin-induced antinociception. It is concluded that the inhibition of nitric oxide/cyclic guanosine monophosphate system in the spinal cord potentiates i.c.v. administered morphine-induced antinociception but attenuates i.c.v. beta-endorphin-induced antinociception. The activation of nitric oxide/cyclic guanosine monophosphate system in the spinal cord attenuates i.c.v. administered morphine-induced antinociception but does not affect i.c.v. administered beta-endorphin-induced antinociception.
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PMID:Nitric oxide/cyclic guanosine monophosphate system in the spinal cord differentially modulates intracerebroventricularly administered morphine- and beta-endorphin-induced antinociception in the mouse. 761 52


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