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)

Bicarbonate secretion by duodenal mucosa free of Brunner's glands was titrated in situ in anesthetized rats. Intracerebroventricular infusion of thyrotropin-releasing hormone (0.01-1 microgram/h), bombesin, gastrin-releasing peptide, or corticotropin-releasing factor increased the bicarbonate secretion and the transmucosal electrical potential difference. The increase in secretion in response to thyrotropin-releasing hormone and bombesin was prevented by cervical vagotomy. Intravenous administration of the alpha-adrenoceptor antagonist phentolamine increased the magnitude and duration of the response, suggesting that these two peptides in addition to eliciting vagal stimulation of the duodenal secretion, by sympathetic activation, inhibit the secretion. Intravenous thyrotropin-releasing hormone (3.6 mg/kg) did not affect the secretion, further indicating that effects were elicited within the central nervous system. Intracerebroventricular infusion of cholecystokinin-octapeptide or beta-endorphin had no effect on duodenal bicarbonate secretion or on the potential difference. The latter peptide was a potent stimulant of the secretion when injected intravenously and probably acts at a peripheral site. The central nervous control of duodenal mucosal bicarbonate secretion is thus influenced by some specific peptides that are known to occur in brain tissue, and duodenal protection against acid might be modulated by agents affecting this control.
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PMID:Stimulation of duodenal mucosal bicarbonate secretion in the rat by brain peptides. 222 6

Effects of opioid peptides (beta-endorphin, dynorphin (1-13). alpha-neoendorphin, beta-neoendorphin, leucine-enkephalin, methionine-enkephalin) on the release of thyrotropin-releasing hormone (TRH) from the rat caecum were studied in vitro. The rat caecum was incubated in medium 199 with 1.0 mg/ml of bacitracin (pH 7.4) (medium). The amount of TRH release from the rat caecum into the medium was measured by radioimmunoassay. The immunoreactive TRH (ir-TRH) release from the rat caecum was inhibited significantly in a dose-related manner with the addition of opioid peptides. The inhibitory effects of opioid peptides on ir-TRH release from the rat caecum were blocked with an addition of naloxone. The elution profile of acid-methanol-extracts of rat caecum on Sephadex G-10 was identical to that of synthetic TRH. The findings suggest that opioid peptides inhibit TRH release from the rat caecum in vitro.
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PMID:Effects of opioid peptides on thyrotropin-releasing hormone release from the rat caecum in vitro. 250 16

The localization of thyrotropin-releasing hormone-immunoreactive structures was investigated in the hypothalamo-hypophyseal complex of the frog, Rana ridibunda, by light and electron microscopy using the conventional indirect immunoperoxidase technique and the immuno-gold technique, respectively. The localization of mesotocin-, vasotocin- and neurophysin-immunoreactive elements was compared to that of thyrotropin-releasing hormone either by comparing homologous fields on serial sections or by staining the same section with two different antibodies. Thyrotropin-releasing hormone-immunoreactive perikarya occurred mainly in the anterobasal periventricular area and dorsal extension of the preoptic nucleus, and in the lateral zone of the infundibular nucleus. In the anterobasal preoptic nucleus, the distribution of thyrotropin-releasing hormone-immunoreactive perikarya partially overlapped that of vasotocin- and mesotocin-containing neurons; however, co-localization of thyrotropin-releasing hormone with either nonapeptide could not be detected there. In contrast, in the caudal extension of the preoptic nucleus, thyrotropin-releasing hormone- and mesotocin-like immunoreactivities were frequently co-localized in the same neurons. In the external zone of the median eminence, abundant networks of thyrotropin-releasing hormone- and vasotocin-immunoreactive nerve fibers were found in the vicinity of portal capillaries, while mesotocin-immunoreactive axons were only found in the internal zone. Using the immuno-gold technique at the electron microscopic level, three distinct thyrotropin-releasing hormone-immunoreactive systems were identified in the median eminence-neurointermediate lobe complex. (1) In the external zone of the median eminence, a conspicuous population of pericapillary endings contained 100-nm dense core vesicles immunoreactive solely for thyrotropin-releasing hormone. (2) In the neural lobe of the pituitary, thyrotropin-releasing hormone immunoreactivity occurred on secretory vesicles in a subpopulation of the mesotocinergic axons containing 160-nm secretory granules; co-localization with vasotocin was never seen. (3) In the intermediate lobe, thyrotropin-releasing hormone- and mesotocin (or neurophysin I)-immunoreactivities were systematically found in the same 120-nm dense core vesicles; these thyrotropin-releasing hormone-/mesotocin-immunoreactive axon terminals frequently made synaptic contacts with melanotropic cells. The possible modulatory effect of mesotocin on thyrotropin-releasing hormone-induced alpha-melanocyte-stimulating hormone secretion was investigated using perifused frog neurointermediate lobes. Administration of graded doses of mesotocin (from 10(-10) to 10(-5) M) did not affect the spontaneous release of alpha-melanocyte-stimulating hormone. In addition, mesotocin (10(-7) and 10(-6) M) did not modify thyrotropin-releasing hormone-evoked alpha-melanocyte-stimulating hormone release.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Three distinct thyrotropin-releasing hormone-immunoreactive axonal systems project in the median eminence-pituitary complex of the frog Rana ridibunda. Immunocytochemical evidence for co-localization of thyrotropin-releasing hormone and mesotocin in fibers innervating pars intermedia cells. 251 4

In this study we have investigated the presence of nerve fibers containing dopamine, thyrotropin-releasing hormone (TRH) and neuropeptide Y (NPY) in the pars intermedia of the crested newt and we have examined the possible effect of these neurohormones on the release of alpha-melanotropin (alpha-MSH) by neurointermediate lobes in vitro. By means of immunohistochemistry, we observed the presence of tyrosine hydroxylase (TH)-immunoreactive fibers in the pars intermedia of the crested newt. Using a specific antiserum to dopamine, these fibers appeared to be mainly dopaminergic in nature. Unlike anurans, urodele amphibians do not exhibit TRH or NPY-like immunoreactivity in the pars intermedia. A perifusion system technique for newt pituitaries was developed to investigate the effect of dopamine, TRH and NPY on alpha-MSH secretion. Administration of increasing concentrations of dopamine (from 10(-9) to 10(-5)M) induced a dose-related inhibition of alpha-MSH release. This inhibitory effect was mimicked by the dopamine agonist apomorphine (10(-6)M). In contrast, the secretory activity of the newt pars intermedia was not affected by administration of synthetic TRH or NPY (up to 10(-7) and 10(-6)M, respectively). These results indicate that the neurotransmitter dopamine likely plays a pivotal role in the regulation of melanotropin secretion in urodele amphibians.
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PMID:Innervation of the pars intermedia and control of alpha-melanotropin secretion in the newt. 251 95

The purpose of the present investigation was to examine the receptor specificity of dopamine inhibition of gonadotropin (GtH) and alpha-melanocyte-stimulating hormone (alpha-MSH) release from the goldfish (Carassius auratus) pituitary in vitro. Pars distalis (PD) and neurointermediate lobe (NIL) fragments of the goldfish pituitary were superfused in vitro under various experimental paradigms; eluate from PD and NIL fragments was analyzed for (GtH) and (alpha-MSH), respectively. Spontaneous GtH release from PD fragments was relatively constant over 6 hr; continuous superfusion with dopamine reversibly inhibited spontaneous GtH release with an estimated ED50 of 10(-4.4) M. Domperidone, a specific D-2 receptor antagonist, reversed the inhibitory action of dopamine and increased spontaneous GtH release. Acute treatment of PD fragments with salmon GnRH (sGnRH) stimulated GtH release; dopamine inhibited GtH release from similarly treated fragments with an ED50 of 10(-7.5) M. The spontaneous release of alpha-MSH from NIL fragments was relatively constant over 6 hr; continuous superfusion with dopamine reversibly inhibited this release with an ED50 of 10(-7.2) M. Acute treatment of NIL fragments with thyrotropin-releasing hormone (TRH) caused acute dose-related increases in alpha-MSH release with an ED50 of 10(-8.2) M; dopamine reversibly inhibited alpha-MSH release from similarly treated fragments with an ED50 of 10(-7.7) M. Both stereoisomers of apomorphine, a dopamine agonist, inhibited GtH release from PD fragments treated with sGnRH; in contrast, alpha-MSH release from NIL fragments treated with TRH was stereospecifically inhibited by (-)-apomorphine, but not by (+)-apomorphine. Domperidone reversed (ED50 = 10(-6.6) M) dopamine (10(-6.3) M) inhibition of GtH release from PD fragments treated with sGnRH. In NIL fragments, the inhibitory action of dopamine (10(-6.3) M) was reversed by domperidone (ED50 = 10(-5.5) M), which restored the acute alpha-MSH release response to TRH. These results suggest the involvement of a low-affinity dopamine/neuroleptic receptor in dopamine inhibition of GtH and alpha-MSH release from the pituitary of the goldfish.
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PMID:Dopamine inhibition of gonadotropin and alpha-melanocyte-stimulating hormone release in vitro from the pituitary of the goldfish (Carassius auratus). 252 42

The action of thyrotropin-releasing hormone (TRH) on melanotrope cells maintained in primary culture was studied with biochemical and electrophysiological techniques. TRH effects on polyphosphoinositide (PPI) breakdown was measured in [3H]myoinositol labelled cells maintained in suspension for 24 hours or in primary culture. TRH (50 nM) or its potent analogue (3Me-His2)-TRH increased total PPI levels by 50-125% in separate experiments after 30 min of treatment whereas corticotropin-releasing hormone (CRF) was without effect. The effect of TRH was dose-dependent (ED50 = 5 nM), the maximal effect being reached with 50 nM TRH. Using the patch-clamp technique in the cell-attached configuration spikes were recorded extracellularly. In 6 of the 13 cells tested, (3Me-His2)-TRH (10 nM) elicited an increase in the spontaneous spiking rate. Furthermore, TRH (50 nM) increased melanocyte-stimulating hormone (alpha-MSH) secretion 2-fold after 8 h of treatment. These results suggested that TRH activated phospholipase C and electrical activity in melanotrope cells; the resulting phosphoinositide breakdown and increase in intracellular free Ca2+ ultimately led to a stimulation of hormone release.
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PMID:Thyrotropin-releasing hormone stimulates porcine melanotrope cells in primary culture. 254 Apr 65

To explore and to compare hypothalamic-pituitary-somatotropic (HPS), hypothalamic-pituitary-thyroid (HPT) and hypothalamic-pituitary-adrenocortical (HPA) axis function in depression, 30 subjects (15 patients with a major depressive episode and individually matched controls) received 50 micrograms growth hormone-releasing hormone-44 amide at 9:00, 200 micrograms thyrotropin-releasing hormone (TRH) at 9:00 and 100 micrograms human corticotropin-releasing hormone (CRH) at 18:00 on consecutive days as an i.v. bolus dose. Compared with controls, depressed patients showed blunted growth hormone (GH) responses to GHRH, decreased TRH-induced thyrotropin (TSH) release and reduced corticotropin (ACTH) but normal cortisol secretion following CRH. ACTH secretion following CRH and TRH-induced TSH release were positively correlated across depressed patients and controls but no significant correlations between GH responses to GHRH and TRH-induced TSH release or ACTH and cortisol secretion following CRH administration were demonstrated. Our findings suggest that altered HPT and HPA axis function associated with depression are triggered by factors that are at least partly different from those that cause HPS system dysfunction. We conclude that the pathophysiological process resulting in aberrant neuroendocrine secretory dynamics associated with depression may primarily occur at a suprapituitary site, and that HPS, HPT and HPA axis dysfunction may be precipitated by complex central and peripheral regulatory mechanisms involving largely independent factors.
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PMID:Endocrine responses to growth hormone-releasing hormone, thyrotropin-releasing hormone and corticotropin-releasing hormone in depression. 254 70

Seven cases with uremia (6 men, 1 woman, mean age = 55.6 +/- 2.2 years) were studied with four combined hypothalamic releasing hormones (corticotropin-releasing hormone, CRH; luteinizing hormone-releasing hormone, LHRH; thyrotropin-releasing hormone, TRH; and growth hormone-releasing hormone, GHRH) for assessment of anterior pituitary functions. The mean basal levels of corticotropin (ACTH, 22.4 +/- 5.2 pg/ml), thyrotropin (TSH, 2.4 +/- 0.6 microU/ml), and follicle stimulating hormone (FSH, 26.0 +/- 3.4 mIU/ml) in uremic patients were not significantly different from those (34.0 +/- 3.5 pg/ml, 2.0 +/- 0.4 microU/ml, and 23.2 +/- 6.4 mIU/ml) of controls (5 men, 1 woman, mean age = 54 +/- 2.5 years), but the ACTH and TSH responses to the releasing hormones were significantly lower than those of the controls. The mean basal levels of luteinizing hormone (LH, 70.7 +/- 16.3 mIU/ml), cortisol (9.8 +/- 1.2 micrograms/dl) and prolactin (109.3 +/- 23.2 ng/ml) in uremic patients were significantly higher than those of normals (27.3 +/- 6.6 mIU/ml, 6.5 +/- 0.7 micrograms/dl and 15.7 +/- 3.4 ng/ml), while suppressed LH, cortisol and prolactin responses to the releasing hormones were observed in the uremic group. The mean basal growth hormone (GH) level in uremic patients (3.1 +/- 0.4 ng/ml) was not significantly different from that (2.8 +/- 0.7 ng/ml) of normals, but the GH response to the releasing hormones was significantly higher than that of controls. These results show pituitary dysfunction, such as blunted ACTH, TSH, LH and prolactin response, exists in uremic patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Anterior pituitary functions in patients with uremia tested by stimulation with four combined hypothalamic releasing hormones. 256 85

The coexistence of varying combinations of substance P (SP), somatostatin (SOM), thyrotropin-releasing hormone (TRH) and met-enkephalin-Arg-Gly-Leu (ENK) with 5-hydroxytryptamine (5-HT) as semiquantitatively revealed by immunocytochemistry in neuronal perikarya of the raphe pallidus et obscurus in the guinea-pig was analyzed. SOM coexisted most frequently with 5-HT, followed by SP, ENK and TRH. Many 5-HT neurons were immunoreactive to 2 or more peptides such as SP/SOM, SOM/ENK, SP/ENK, SOM/TRH, SP/TRH or SOM/SP/ENK. Most of these neurons were shown to project to the spinal cord by retrograde HRP labeling combined with immunocytochemistry. After hemisection of the cervical spinal cord at the C5 level, ENK and 5-HT immunoreactive nerve terminals in the ipsilateral intermediolateral nucleus of the thoracic spinal cord were decreased in number. The results indicate that neurons in the raphe pallidus et obscurus projecting to the spinal cord can be classified into subpopulations according to which peptides coexist with 5-HT, and may have different functions.
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PMID:Coexistence of varying combinations of neuropeptides with 5-hydroxytryptamine in neurons of the raphe pallidus et obscurus projecting to the spinal cord. 257 20

Clinical and laboratory evidence indicates that the brain exerts major control on the gastrointestinal tract. Specific brain loci and circuits that send efferent viscerotropic projections to the gut have been described. A variety of aminergic and peptidergic neurotransmitters have been shown to occur along these cerebrogastrointestinal pathways and to influence motor and secretory functions of the gut. Some of the newly identified peptides have been shown to influence the development of gastroduodenal ulcers. Findings with thyrotropin-releasing hormone (TRH) indicate that this endogenous tripeptide induces a full spectrum of gut effects, prominent among which is production of gastric ulcers. By contrast, other peptides including beta-endorphin, neurotensin, and bombesin induce gut effects opposite to those of TRH, namely, inhibition of gastric acid and motility and prevention of experimental ulcers. These laboratory findings suggest that ulcer disease may represent a brain-driven event, which may be the result of a neurochemical imbalance within the brain. Further neurobiological research will generate additional data on brain-gut interactions and will probably disclose new information to explain certain functional and organic disorders of the gut.
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PMID:Neurobiology of brain-gut interactions. Implications for ulcer disease. 257 55


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