Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Morphine given systemically or centrally increases the plasma concentration of cyclic GMP in male, ddY strain mice. Normorphine also increased the plasma cyclic GMP level, whereas the same dose of ketocyclazocine and SKF 10,047 had no effect. The effect of morphine on plasma cyclic GMP was mimicked by opioid peptides such as (D-Ala2, Met)-enkephalinamide, FK 33,824 or beta-endorphin. The effect of morphine and opioid peptides on plasma cyclic GMP was antagonized by naloxone, indicating the involvement of the opiate receptor. The increase in plasma cyclic GMP elicited by morphine was abolished by vagotomy and pretreatment with hexamethonium and atropine and was partly inhibited by pretreatment with phentolamine. Adrenalectomy and pretreatment with propranolol, which inhibited the increase in plasma cyclic AMP level elicited by morphine (Muraki et al., 1979), did not alter the cyclic GMP response to morphine. The development of tolerance to the cyclic GMP increase was observed in morphine-tolerant/dependent mice. These results suggest that morphine increases the plasma cyclic GMP level by activating the preganglionic parasympathetic tone via the stimulation of the opiate receptors, thereby increasing the generation of cyclic GMP through the muscarinic receptors on the effector cells.
 ...
PMID:Mechanism of morphine in increasing plasma cyclic GMP level in male mice. 629 63

The effect of cholecystokinin octapeptide (CCK-8) on the release of beta-endorphin-like immunoreactivity (beta-EpLI) in rats was studied in vivo and in vitro. Intravenous injection of 5 micrograms/100 g body weight of CCK-8 resulted in significant increase in the plasma beta-EpLI level after 10 and 20 min. CCK-8 at concentrations of 10(-10) - 10(-6) M also caused dose-dependent stimulation of beta-EpLI release from dispersed cells of rat anterior pituitary. However, CCK-4 and desulfated CCK-8 had no effect. On gel chromatography, the beta-EpLI released by incubation of the cells with 10(-8) M CCK-8 separated into two components, eluted in the same positions as human beta-lipotropin and human beta-endorphin, respectively. CCK-8 did not stimulate beta-EpLI release in Ca++-free medium. A 23187 at concentrations of 10(-6) - 10(-3) M caused dose-dependent stimulation of beta-EpLI release from the cells. Addition of 2 X 10(-3) M CoCl2, 10(-3) M verapamil or 10(-7) M dexamethasone to the incubation medium inhibited CCK-8-induced beta-EpLI release from the cells. Dibutyryl cyclic GMP (3 X 10(-3) M) inhibited CCK-8-induced beta-EpLI release from the cells. Ouabain (10(-5) M) also stimulated beta-EpLI release but its effect was not additive with that of CCK-8. These results indicate that CCK-8 acts directly and specifically on anterior pituitary cells to stimulate beta-EpLI release and that calcium ion is involved in the mechanism of this effect.
 ...
PMID:In vivo and in vitro effects of cholecystokinin octapeptide on the release of beta-endorphin-like immunoreactivity. 630 91

Septal kindling was associated with an inhibition of the post hoc phosphorylation of several synaptic plasma membrane proteins of rat hippocampus. In control rats, the 32P incorporation into proteins of molecular weights 50,000, 58,000, and 60,000 was markedly stimulated by combined calcium/calmodulin, whereas in kindled animals, the response to combined calcium/calmodulin was reduced. Calcium alone, cAMP, or cGMP modulated 32P incorporation into several synaptic plasma membrane proteins but did not differentiate control from kindled tissues. Both control and kindled rats showed nonspecific inhibition of calcium/calmodulin-stimulated phosphorylation in the post hoc assay by corticotropin and by [Leu]enkephalin. The differences between control and kindled animals were most striking in hippocampus and in the amygdaloid-entorhinal area; less pronounced in cortex, basal ganglia, and brain stem; and not significant in cerebellum, a region where kindling cannot be elicited. An 8-wk period of rest after kindling did not reduce these changes, suggesting that they may be a persistent as the kindling behavior itself.
 ...
PMID:Kindling alters the calcium/calmodulin-dependent phosphorylation of synaptic plasma membrane proteins in rat hippocampus. 632 92

(+)-cis-Dioxolane (0.5-2 micrograms), a muscarinic receptor agonist, given intracerebroventricularly (i.c.v.) produced a dose-dependent inhibition of the tail-flick response in male ICR mice. (+)-cis-Dioxolane given i.c.v. at a subanalgesic dose (0.25 micrograms), selectively potentiated the antinociceptive response induced by i.c.v. administered beta-endorphin, an epsilon-opioid receptor agonist, but not morphine or [D-Ala2,NMePhe4,Gly5-ol]enkephalin (DAMGO), mu-opioid receptor agonists, [D-Pen2,D-Pen5]enkephalin (DPDPE), a delta receptor agonist, or trans(+/-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]- benzeneacetamide methane sulfonate (U50,488H), a kappa-opioid receptor agonist. The antinociceptive response induced by (+)-cis-dioxolane given i.c.v. was attenuated by i.c.v. treatment with N omega-nitro-L-arginine (1 microgram), hemoglobin (120 micrograms) or methylene blue (10 micrograms). The antinociception induced by carbachol given i.c.v. was also antagonized by the i.c.v. treatment with N omega-nitro-L-arginine (1 microgram). However, the same treatment with N omega-nitro-L-arginine, hemoglobin or methylene blue did not affect the beta-endorphin-induced antinociception. The potentiation of beta-endorphin-induced antinociception by (+)-cis-dioxolane was reversed by i.c.v. treatment with N omega-nitro-L-arginine (1 microgram), hemoglobin (120 micrograms) or methylene blue (10 micrograms). On the other hand, the antinociceptive response induced by (+)-cis-dioxolane (1 microgram) given i.c.v. was potentiated by i.c.v. administered L-arginine (20 micrograms) but not D-arginine (20 micrograms). Dibutyryl cyclic GMP at 0.5-2.0 micrograms given i.c.v. produced an antinociceptive response and at subanalgesic dose (0.1 microgram) potentiated i.c.v. beta-endorphin-induced antinociception.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Role of nitric oxide/cyclic GMP in i.c.v. administered beta-endorphin- and (+)-cis-dioxolane-induced antinociception in the mouse. 781 87

Although C-type natriuretic peptide (CNP) has been shown to exist at the highest concentration in the anterior pituitary in rat tissues, its physiological role(s) there is (are) not clear. In this study, we report a novel function of CNP examined with anterior pituitary-derived cell lines, GH3 and AtT20/D16v-F2. Both CNP and atrial natriuretic peptide (ANP) increased cellular cGMP levels in both cell lines in dose-dependent manners. CNP, but not ANP, stimulated growth hormone (GH) release from GH3 cells. In contrast, neither ANP nor CNP had any significant effect on the corticotropin release from AtT20/D16v-F2 cells. An activator for cGMP-dependent protein kinase (cGK), dibutyryl cGMP, mimicked the stimulation of GH release from GH3 cells by CNP. Constitutive GH release from GH3 cells was greatly diminished in the presence of inhibitors for cAMP-dependent protein kinase, while stimulative GH release by CNP was not affected. However, inhibitors which can block cGK almost completely diminished the stimulative effect of CNP. An inhibitor for protein kinase C did not show any effect on either constitutive or CNP-stimulative GH release. Our observations indicate that the stimulation of GH release from GH3 cells by CNP is mediated mainly by the cGK signal-transduction pathway, not by cAMP-dependent protein kinase or protein kinase C, through a CNP-specific receptor (possibly ANP-B receptor). Thus, CNP may act as a local modulator in the anterior pituitary.
 ...
PMID:C-type natriuretic peptide stimulates secretion of growth hormone from rat-pituitary-derived GH3 cells via a cyclic-GMP-mediated pathway. 802 May 2

The melanocyte-stimulating hormone (alpha-MSH) used at 10(-6)-5 x 10(-8) M concentrations inhibited the growth of amelanotic cells of human malignant melanoma BRO and influenced cell morphology without any effect on melanization or tyrosinase activity. Inhibition of tumour cell growth was accompanied by marked elevation of intracellular cAMP levels but not that of cGMP. Dibutyryl-cAMP and the cAMP-dependent protein kinase A inhibitor also inhibited the cell growth. alpha-MSH increased mono-, di- and 1.4.5-myoinositol triphosphate concentrations and influenced the activities of phosphatidylinositol kinase and phosphatidylinositol-4-phosphate kinase determining phosphatidylinositol-4-phosphate kinase and phosphatidylinositol-4.5-diphosphate levels. Myoinositol phosphate concentrations changed on a second scale and levelled off by the 3rd-5th min, whereas that of cAMP increased drastically by the 30th min.
 ...
PMID:[Melanocyte-stimulating hormone induces growth of human malignant melanoma amelanotic cells with a change in cAMP, phosphatidylinositols, and inositol phosphate concentration]. 838 47

Nitric oxide (NO) donors such as sodium nitroprusside (SNP, 0.01-1 micrograms) or 3-morpholino-sydnonimine (SIN-1, 0.1-10 micrograms) administered intracerebroventricularly (i.c.v) produced a dose-dependent potentiation of beta-endorphin-induced antinociception assessed by the tail-flick test in ICR mice. The same i.c.v. treatment with SNP or SIN-1 did not affect the antinociception induced by mu-, delta-, or kappa-opioid receptor agonists. The goal of the present study was to determine if the potentiation of the beta-endorphin-induced antinociception by NO donors is mediated by the activation of NO-cGMP system. Co-administration of hemoglobin (30-120 micrograms) or methylene blue (1.25-5 micrograms), but not N omega-nitro-L-arginine (1-5 micrograms) given i.c.v. dose-dependently attenuated the potentiating effects of SNP or SIN-1 on beta-endorphin-induced antinociception. However, the same i.c.v. treatments of mice with hemoglobin, methylene blue or N omega-nitro-L-arginine did not directly affect the i.c.v. administered beta-endorphin-induced antinociception. On the other hand, the treatment of mice with a combination of NO donor (SNP, 0.1 micrograms or SIN-1, 1 microgram) and zaprinast (a cGMP phosphodiesterase inhibitor, 1 microgram) further potentiated beta-endorphin-induced antinociception. These results indicate that the potentiating effect of SNP or SIN-1 on beta-endorphin-induced antinociception is mediated by the increased production of NO-cyclic GMP in the brain. However, the NO-cGMP system is not directly involved in the beta-endorphin-induced antinociception.
 ...
PMID:Activation of a NO-cyclic GMP system by NO donors potentiates beta-endorphin-induced antinociception in the mouse. 871 39

Adrenocorticotropic hormone (ACTH) increases cAMP and cGMP concentrations in both adrenal and lymphoid cells, and requires extracellular Ca to have biological activity. The requirement for Ca has been difficult to characterize in terms of the channel identity and whether the committing step for steroidogenesis in the adrenal cells requires Ca. In lymphocytes, ACTH has a biphasic effect on functions such as proliferation and immunoglobin secretion. Current information is consistent with suppressive effects of high ACTH concentrations being mediated by cAMP. Stimulatory effects of ACTH concentrations are hypothesized to be mediated by Ca uptake. This review will discuss the localization of Ca signals to discrete domains within cells and the receptor- and tissue-specificity of their subcellular distribution. Considering the diversity of possible mechanisms, a hypothesis for the role of ACTH-stimulated Ca uptake during mitogen activation of T-cell lymphocytes will be presented.
 ...
PMID:Calcium uptake by ACTH-stimulated lymphocytes: what is the physiological significance? 874 71

Nitric oxide (NO) is now recognized as a diffusible messenger molecule that normally augments intercellular communication in the central nervous system, but is neurotoxic if released in excessive amounts. NO is synthesized from L-arginine by the Ca2+/calmodulin-dependent neuronal isoform NO synthase (NOS) localized in sub-populations of neurons throughout the brain, including the hypothalamus. In the hypothalamus, NO stimulates the release of GnRH, the primary neurohormone governing reproduction in mammals. Although the excitatory amino acid, glutamate, acting through the N-methyl-D-aspartate (NMDA) receptor is believed to be responsible for stimulation of NO release, the neuronal system(s) that inhibits NO efflux is unknown. As the endogenous opioids, primarily beta-endorphin (betaEND), exert a tonic restraint on GnRH secretion, we sought evidence for a possible functional link between betaEND and NOS pathways in the hypothalamus. We observed that restraining the opioid influence with the opiate receptor antagonist, naloxone, in intact, but not in castrated, rats rapidly augmented extracellular cGMP/NO efflux in the medial preoptic area, where GnRH, NOS, and betaEND immunoreactive pathways are coextensive. Pituitary LH secretion increased in conjunction with this augmented cGMP/NO response and pretreatment with the mu opiate receptor agonist, morphine, suppressed these naloxone-induced responses. Further, visualization of hypothalamic sections immunostained for both betaEND and NOS revealed betaEND-immunoreactive axon terminals in close proximity to NOS-positive cell bodies and dendrites in a number of hypothalamic subdivisions, including the medial preoptic area. These close appositions represented conventional synapses between betaEND nerve terminals and NOS-positive perikarya and dendrites under the electron microscope. Clearly, the experimental data, corroborated by morphological evidence, point to a direct inhibitory control of betaEND on NOS-immunoreactive neurons in monitoring cGMP/NO release. These findings together with the previous observations that the glutamate neurotransmitter acting through NMDA receptors located on NOS-immunopositive cells stimulates cGMP/NO efflux and plasma LH selectively in intact rats document the existence of a dual control comprised of the excitatory NMDA and the inhibitory mu opiate receptors in modulating cGMP/NO release, a response also directed by gonadal steroids. This new knowledge of an inhibitory opioid influence on cGMP/NO release is probably extremely important both in the generation of periodicities in GnRH secretion that underlie hypothalamic control of reproduction and in protecting against neurotoxic overstimulation of NO release by excitatory amino acids.
 ...
PMID:Evidence showing that beta-endorphin regulates cyclic guanosine 3',5'-monophosphate (cGMP) efflux: anatomical and functional support for an interaction between opiates and nitric oxide. 907 13

On one hand, it has been demonstrated that the exposure of rat brain slices containing caudate putamen and accumbens nuclei to alpha-MSH brings about an increase in cAMP. This increase is affected when dopamine is present in the incubation medium. On the other hand, an interaction of melanotropinergic-like peptides with acetylcholinergic drugs has been showed to be similar to the one observed with dopamine. In this study we have intended to measure cGMP or IP3 in response to alpha-MSH, and also to study the interaction with cholinergic drugs by measuring the second messengers recently mentioned. cGMP and IP3 have been measured in tissues and medium in their response to the effect of alpha-MSH alone or in the presence of the peptide plus pilocarpine (selective muscarinic agonist) or atropine (selective muscarinic antagonist). None of them modified the cGMP levels when compared with the control group. The exposure of rat brain slices containing CP and Acc nuclei to alpha-MSH resulted in an increase in IP3 levels. Pilocarpine by itself brought about an increase of IP3 only when the highest doses was used. Atropine did not modify the IP3 content. However, when slices were exposured to both alpha-MSH and pilocarpine, IP3 content was similar to control values. The blockage of the muscarinic receptor with atropine blocked the IP3 increase induced by alpha-MSH as well. Therefore, we assume that alpha-MSH does not induce changes in cGMP but it does change the IP3 levels, probably acting at the muscarinic receptor level.
 ...
PMID:Effects of alpha-MSH and cholinergic agents on cGMP and IP3 levels in rat brain slices. 920 20


<< Previous 1 2 3 4 5 6 Next >>