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)

Intact adult male rats fed an alcohol [ethanol (EtOH)] diet for 10 days show blunted adrenocorticotropic hormone (ACTH) release in response to immune signals such as the cytokine interleukin-1 beta (IL-1 beta) and endotoxin [lipopolysaccharide (LPS)], as well as to physical stress (mild electroshocks). The mechanisms responsible for this effect remain poorly understood, but we have recently reported that decreased pituitary responsiveness to vasopressin (VP) might play a role. In naive rats, nitric oxide (NO) exerts a restraining influence on the response of the hypothalamic-pituitary (H-P) axis to cytokines and VP. The ability of long-term EtOH treatment to increase glutamate receptors, and thus NO formation, prompted us to test the hypothesis that abnormally high NO concentrations might modulate the influence of the drug. Blockade of the activity of NO synthase (NOS), the enzyme responsible for NO formation, with the arginine derivative L-N omega nitro-L-arginine-methylester (L-NAME), augmented the ACTH response to IL-1 beta or LPS in both control (C) and EtOH-fed (E) rats. Indeed, after L-NAME treatment, ACTH concentrations were statistically comparable in C and E animals injected with endotoxin or a large dose of IL-1 beta. VP-induced ACTH secretion also became comparable in both experimental groups after blockade of NOS activity. In contrast, the decreased response of the H-P axis of E animals to shocks was only slightly ameliorated, compared with that of C rats. It is therefore possible that changes in the NOergic tone induced by alcohol play a role in the decreased response of the H-P axis to cytokines, possibly in part by altering the stimulatory action of VP on the corticotrophs. On the other hand, in E rats NO seems to exert only a minimal influence on the central nervous system circuits activated by shocks.
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PMID:Adult male rats exposed to an alcohol diet exhibit a blunted adrenocorticotropic hormone response to immune or physical stress: possible role of nitric oxide. 874 13

Heme oxygenase is an essential enzyme in the heme catabolism that produces carbon monoxide (CO). This study was designed to examine the expression of two heme oxygenase isozyme mRNAs in the human brain and to explore the involvement of nitric oxide (NO) and various neuropeptides in the regulation of their expression. Northern blot analysis showed the expression of heme oxygenase-1 and heme oxygenase-2 mRNAs in every region of the brain examined, with the highest levels found in the frontal cortex, temporal cortex, occipital cortex, and hypothalamus. In a human glioblastoma cell line, T98G, treatment with any of three types of NO donors--sodium nitroprusside, 3-morpholinosydnonimine, and S-nitroso-L-glutathione--caused a significant increase in the levels of heme oxygenase-1 mRNA but not in the levels of heme oxygenase-2 and heat-shock protein 70 mRNAs. Sodium nitroprusside increased the levels of heme oxygenase-1 protein but not the levels of heat-shock protein 70 in T98G cells. The increase in content of heme oxygenase-1 mRNA caused by sodium nitro-prusside was completely abolished by the treatment with actinomycin D. On the other hand, the levels of heme oxygenase isozyme mRNAs were not noticeably changed in T98G cells following the treatment with 8-bromo cyclic, GMP sodium nitrite, or various neuropeptides, such as calcitonin gene-related peptide, endothelin-1, and corticotropin-releasing hormone. The present study has shown the expression profiles of heme oxygenase-1 and -2 mRNAs in the human brain and the induction of heme oxygenase-1 mRNA caused by NO donors in T98G cells. These findings raise a possibility that the CO/heme oxygenase system may function in concert with the NO/NO synthase system in the brain.
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PMID:Expression of heme oxygenase isozyme mRNAs in the human brain and induction of heme oxygenase-1 by nitric oxide donors. 876 71

Double-label immunocytochemistry was used to investigate the colocalisation of various neuropeptides and the enzymes nitric oxide synthase (NOS) and tyrosine hydroxylase (TH) in intramural ganglia of the human male urinary bladder neck and trigone. Postmortem specimens were obtained from 7 male infants and children ranging in age from 2 mo to 3 y who had died as a result of cot death or accidental trauma. On average 60% of the intramural neurons were non-TH-immunoreactive (-IR) (i.e. presumptive cholinergic) and 40% were TH- and D beta H-IR (i.e. noradrenergic). Within the non-TH-IR population, calcitonin gene-related peptide (CGRP) was found in 65% of cells, neuropeptide Y (NPY) in 90%, nitric oxide synthase (NOS) in 45%, somatostatin (SOM) in 90%, and vasoactive intestinal polypeptide (VIP) in 40%. The corresponding values for the TH-IR neurons were CGRP (54%), NPY (70%), NOS (58%), SOM (73%) and VIP (40%). All the observed bombesin (BOM)-immunoreactivity was colocalised with TH while 90% of VIP and almost all the CGRP was colocalised with NPY. Less than 5% of neurons were immunoreactive for substance P (SP) or met-enkephalin (m-ENK) and some of these also contained TH. Varicose nerve fibres were seen in close proximity to some of the intramural neurons, the majority of such varicosities showing immunoreactivity to CGRP, VIP or TH. Less common were pericellular varicosities immunoreactive to NPY, SOM or SP. These results demonstrate the neurochemical heterogeneity of intramural neurons in the human bladder neck and provide indirect evidence for the complexity of the peripheral innervation of the human urinary bladder.
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PMID:A double-label immunohistochemical study of intramural ganglia from the human male urinary bladder neck. 903 88

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.
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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

In this paper we report a time-course study of development of experimental allergic encephalomyelitis in Lewis rats, by monitoring neuroendocrine regulation of the hypothalamus-pituitary-adrenal axis through corticotropin-releasing hormone mRNA expression, inflammatory cellular infiltrate, macrophagic and neuronal nitric oxide synthase, nerve growth factor (NGF), and NGF p75 and trkA receptors in the brain and spinal cord. We analyzed animals during 20 days after immunization, a time interval that corresponds to the acute immunological phase. We have described a severe, early fall of corticotropin-releasing hormone mRNA expression, which could account for the decreased response of the hypothalamus-pituitary-adrenal axis to inflammatory stress. During this period, an increase of neuronal nitric oxide synthase was observed in the cerebral cortex and spinal cord, and macrophagic nitric oxide synthase positive cells were found in the inflammatory cellular infiltrate, which was abundant in perivascular and submeningeal areas 20 days after immunization. Concomitantly, we found a dramatic up-regulation of NGF receptors on the wall of blood vessels and adjacent neurons in perivascular areas. NGF content also had increased in some brain areas, such as the thalamus, while it had decreased in others, like the spinal cord and medulla oblongata, at time points in which the most serious cellular infiltrate was found.
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PMID:Time-course changes of nerve growth factor, corticotropin-releasing hormone, and nitric oxide synthase isoforms and their possible role in the development of inflammatory response in experimental allergic encephalomyelitis. 909

A systematic search for neuroendocrine (NE) cells in the urogenital organs of the pig was carried out by means of Linder's argyrophil method and immunohistochemical techniques. The occurrence, distribution and immunohistochemical character of NE cells (paraneurons) were studied in the vaginal vestibulum, vagina, uterus, oviduct, ovary, urethra, urinary bladder and ureter. In the vestibular glands paraneurons were found to be the most numerous, while a moderate number of these cells occurred in the uterine horn and in the urethra. A distinctly smaller number of paraneurons was present in the oviduct and only occasional NE cells were observed in the urinary bladder. Immunohistochemistry was performed by using the peroxidase-antiperoxidase procedure. Different subpopulations of paraneurons were distinguishable. Chromogranin A-positive paraneurons were found in the vestibular glands, uterine horns, oviducts, urethra and urinary bladder. Somatostatin positivity was observed in NE cells of the vestibular gland, uterine horn, oviduct and urethra. The subpopulation of serotonin-positive paraneurons was present in the vestibular gland and urethra. Bombesin, vasoactive intestinal polypeptide, cholecystokinin, substance P, nitric oxide synthase, beta-endorphin, insulin, adrenocorticotropic hormone, oxytocin and thyroid-stimulating hormone antibodies gave negative reactions in the studied NE cells.
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PMID:Neuroendocrine cells in the female urogenital tract of the pig, and their immunohistochemical characterization. 909 38

1. Evidence supporting the presence in the invertebrate nervous system of a class of glial cells resembling vertebrate microglia was obtained in the freshwater snail Planorbarius corneus. These cells are easily identified by their immunopositivity to anti-pro-opiomelanocortin (POMC)-derived peptide antibodies. 2. Invertebrate microglia, as in vertebrates, exhibit macrophage-like activity in vivo and in cell cultures. These cells respond to the trauma of ganglionic excision and their organotypic culture by leaving their location around neurons and moving to the lesion site from which they migrate in the culture dish. 3. In vitro, these microglia undergo conformational changes and show phagocytic properties in the presence of bacteria or lipopolysaccharide. The activated cells also express tumor necrosis factor-alpha-like material and an increase in nitric oxide synthase, as shown by immunocytochemistry. 4. The inhibitory effect of morphine on the mobility and phagocytic activity of invertebrate microglia provide additional functional evidence for a possible role of opiate-like compounds in downregulating immunoregulatory processes, as also observed in the circulating immunocytes.
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PMID:Opiate signaling regulates microglia activities in the invertebrate nervous system. 919 91

Nitric oxide (NO) generated by the enzyme nitric oxide synthase (NOS) has been implicated in the regulation of a variety of endocrine functions. A number of biochemical and anatomical studies have demonstrated the presence of neuronal NOS (nNOS) in the neuroendocrine axis and have shown significant effects of NO on the release of hypothalamic and pituitary hormones. Using a C-terminal directed peptide antibody that is specific for nNOS we have found a predominance of nNOS in the neural lobe of the pituitary and in a single layer of epithelial cells, possibly a remnant of Rathke's pouch that form a border between the intermediate lobe and the anterior lobe. Furthermore, we have examined the effect of sodium nitroprusside (SNP), a donor of NO on the secretion of beta-endorphin (beta-EP) from the isolated neuro-intermediate lobe (NIL) of the rat and cultured rat melanotrophs. It was shown that in explant cultures of intact neuro-intermediate lobes, SNP (100 microM) was able to cause an inhibition of beta-EP secretion. In the presence of sulpiride (10 microM), a dopamine D2-receptor antagonist, there was a partial reversal of the SNP effect. On the other hand SNP did not affect beta-EP secretion in primary cultures of melanotrophs that no longer possessed any innervation. Taken together these data suggest that NO has an indirect inhibitory effect on the secretion of beta-EP by the intermediate lobe via the release of dopamine.
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PMID:The involvement of nitric oxide in the secretion of beta-endorphin from the pituitary intermediate lobe of the rat. 924 73

Anesthetized rats were subjected to volume-controlled hemorrhagic shock by stepwise bleeding. Besides cardiovascular and respiratory functions, nitric oxide (NO)-hemoglobin formation in arterial blood was directly evaluated by means of electron spin resonance spectroscopy. During hemorrhagic shock there was a massive increase in NO-hemoglobin, associated with a fall in mean arterial pressure, pulse pressure, respiratory rate and heart rate, and there was a further increase in NO-hemoglobin 15 min after intravenous (i.v.) treatment with saline. All rats died within 30 min. The reversal of the shock condition induced by the i.v. injection of the adrenocorticotropin (ACTH) fragment 1-24 (160 microg/kg, 5 min after bleeding termination) was associated with a prompt disappearance of NO-hemoglobin. Also S-methylisothiourea (3 mg/kg i.v.), a selective inhibitor of inducible NO synthase, provoked a disappearance of NO-hemoglobin and reversal of the shock condition. The present results provide a direct demonstration that volume-controlled hemorrhagic shock is associated with highly increased blood levels of NO, as indicated by increased NO-hemoglobin, and indicate that ACTH-induced reversal of the shock condition is associated with the normalization of NO blood levels, and a parallel improvement of cardiovascular and respiratory functions. This occurs probably through the inhibition of inducible NO synthase, as suggested by the fact that S-methylisothiourea, a selective inhibitor of this NO synthase isoform, produced the same results.
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PMID:Adrenocorticotropin normalizes the blood levels of nitric oxide in hemorrhage-shocked rats. 938 49

We investigated whether NG-nitro-L-arginine methyl ester (L-NAME), a specific inhibitor of nitric oxide synthase (NOS), can modify the stress-induced adrenocorticotropic hormone (ACTH) and corticosterone responses, because we found that immobilization-induced stress increases NOS mRNA and protein levels and enzyme activity in the adrenal cortex. The physiological significance of these phenomena, however, remains unknown. Plasma ACTH and corticosterone levels were determined by radioimmunoassay (RIA) of systemic blood samples and NOS enzyme activity was measured as the rate of [3H]arginine conversion to [3H]citrulline in the presence of tissue homogenate of adrenal cortex separated from the adrenal gland. The NOS enzyme activity in the adrenal cortex of rats pre-injected with saline at 2 h after the 2-h immobilization was significantly higher (P < 0.01) than that in the non-stressed controls. Pre-injection of L-NAME (100 mg/kg, s.c.) almost completely abolished the activity. This dose of L-NAME maintained a significantly elevated plasma corticosterone level (P < 0.05, compared with basal level) even 2 h after the 2-h stress, whereas the plasma corticosterone level in rats pre-injected with saline returned to the basal level at the same time point. Plasma ACTH level in L-NAME-pre-treated rats was higher than that in those pre-treated with saline 2 h after the stress, but the difference was not significant. This dose of L-NAME did not influence plasma ACTH or corticosterone levels under resting conditions without stress. These findings suggest that the stress-induced increase in NO synthesis in the adrenal cortex can modify the stress-induced corticosterone response to facilitate the recovery from the elevated corticosterone secretion by stress in the adrenal cortex to the resting basal level.
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PMID:Modulatory effect of L-NAME, a specific nitric oxide synthase (NOS) inhibitor, on stress-induced changes in plasma adrenocorticotropic hormone (ACTH) and corticosterone levels in rats: physiological significance of stress-induced NOS activation in hypothalamic-pituitary-adrenal axis. 943 97


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