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 antinociceptive and hypothermic effects of intracisternal administration of 11 endogenous neuropeptides and morphine were evaluated in mice. Of the substances tested, only neurotensin (NT) and beta-endorphin exerted significant antinociceptive and hypothermic effects; NT was the most potent in inducing hypothermia whereas beta-endorphin was the most potent antinociceptive agent via this route of administration. Both NT, and beta-endorphin were, on a molar basis, considerably more potent antinociceptive agents than morphine, [Met]enkephalin, or [Leu]enkephalin. NT-induced analgesia and hypothermia both were significantly dose-dependent. Substance P was found to produce significant hyperalgesia and hyperthermia. Bombesin produced a significant hypothermic effect, whereas somatostatin and luteinizing hormone-releasing hormone (luliberin) produced hyperthermia. None of the other peptides studies [bradykinin, thyrotropin-releasing factor (thyroliberin), melanocyte-stimulating hormone release-inhibiting factor (melanostatin), somatostatin, [Met]enkephalin, and [Leu]enkephalin] produced any significant alterations in colonic temperature or response to a noxious stimulus with the doses tested. These data demonstrate that NT and beta-endorphin, two endogenous brain peptides, are potent in inducing hypothermia and in producing an antinociceptive state.
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PMID:Alterations in nociception and body temperature after intracisternal administration of neurotensin, beta-endorphin, other endogenous peptides, and morphine. 29 52

The distribution of peptide hormone-like immunostaining in the gastrointestinal tract of 11 teleost species was investigated by immunofluorescence. Cells immunoreactive for somatostatin were found in the glandular epithelium of the stomach of four species and in the epithelium of the pyloric appendage of one species. The mid-gut epithelium contained cells reactive with antibodies to glucagon (three species), gastrin (five species), pancreatic polypeptide (five species), and substance P (two species). Cells immunoreactive for met-enkephalin were found in the epithelium of both the mid-gut and the stomach of six species. In six species in which the endocrine pancreas was investigated, insulin-, glucagon-, and somatostatin-like immunoreactivity was observed. Pancreatic polypeptide was definitely localised by immunostaining in cells of the endocrine pancreas of only one out of three species examined. Vasocative intestinal polypeptide-, neurotensin-, bombesin-, and enkephalin-like immunoreactivity was identified in the gastrointestinal nerve fibres in various species. In view of the considerable species variation found, caution should be exercised in generalising about the peptides present in the gastrointestinal tract of fish.
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PMID:Peptide hormone-like immunoreactivity in the gastrointestinal tract and endocrine pancreas of eleven teleost species. 38 3

The hypothalamic hormones arginine-vasopressin (AVP), oxytocin (OXT), somatostatin (SOM), and luteinizing hormone-releasing hormone (LHRH) were localized in the rat neurohypophysis by the use of semithin serial sections and the unlabeled antibody enzyme method. Clusters of AVP fibres are present within the central region of the neural lobe, clusters of OXT fibres mainly in the peripheral part. The AVP fibres enter bilaterally into the neural lobe. The results call into question previous reports on the presence of AVP on receptors in the pars intermedia cells, since incubation with anti-AVP resulted in similar staining in the pars intermedia of the Wistar and homozygous Brattleboro rat, a mutant strain deficient in AVP. The same intermediate lobe cells are stained after incubation of serial sections with anti-AVP and anti-alpha-melanocyte-stimulating hormone (alpha-MSH). This staining of anti-AVP could be removed by solid phase absorption to alpha-MSH and is thus most probably due to cross reaction with alpha-MSH. SOM fibres appear to be present in the peripheral parts of the proximal neurohypophysial stalk and mainly lateral in its more distal parts. In the neural lobe they rapidly decrease in number, although some fibres continue into the distal part of the neural lobe, running bilaterally and situated adjacent to the pars intermedia. The SOM staining within magnocellular elements, which has been reported in the literature, can most probably be explained by cross reaction of anti-SOM with neurophysins. LHRH fibres are very scarce in the neurohypophysial stalk and absent in the neural lobe.
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PMID:The localization of oxytocin, vasopressin, somatostatin and luteinizing hormone releasing hormone in the rat neurohypophysis. 39 93

Complementing cytochemical and ultrastructural studies, immunocytochemistry may be used to define, in terms of immunoreactivity, the nature of the polypeptide(s) made and stored in the cells of the endocrine pancreas, islet or otherwise. Immunoserums are applied to histological sections after fixation of the material in Bouin's fluid, and in accordance with four protocols: indirect immunofluorescence, immuno-enzymatic technique, variants in prolonged primary incubation and the method of soluble peroxidase-antiperoxidase complexes. Certain precautions are essential for correct interpretation. In the adult, four essential immunoreactions, corresponding to hormones or "local hormones" are regularly detected:insulin, pancreatic glucagon, somatostatin, pancreatic polypeptide. The cytochemical and ultrastructural characteristics of the cells involved are known (B, A and D cells for the first three specificities). C-peptide immunoreactivity is easily identified, but other immunoreactivities are more irregular or contested: gastrin, cholecystokinin, vasoactive intestinal peptide, ACTH, met-enkephalin.
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PMID:[Practical immunocytochemistry of the endocrine pancreas]. 39 37

Somatostatin (SRIF) has been tested for its actions on the central nervous system to affect glucoregulation. In doses ineffective when given systemically , SRIF and SRIF analogs given intracisternally (ic) reduce hyperglycemia and hyperglucagonemia after ic bombesin administration. The SRIF analog, des-AA1, 2, 4, 5, 12, 13-[D-Trp8]SRIF, decreases plasma insulin and elevates plasma glucose and glucagon when given systemically. However, when given ic, this peptide prevents the rise in glucose and glucagon after ic bombesin administration and is 10 times more potent than SRIF in reducing bombesin-induced hyperglycemia. Other analogs of SRIF and various unrelated peptides were found to be ineffective in reducing bombesin-induced hyperglycemia. des-AA1, 2, 4, 5, 12, 13-[D-Trp]SRIF prevented the hyperglycemia induced by surgical stress or by ic administration of beta-endorphin or carbacol. des-AA1, 2, 4, 5, 12, 13-[D-Trp]SRIF given ic did not prevent hyperglycemia induced by systemic administration of epinephrine, arginine, or glucagon. These studies suggest that SRIF and its analogs may act within the brain to affect glucoregulation.
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PMID:Somatostatin: central nervous system actions on glucoregulation. 44 91

Somatostatin (SS) inhibits in a dose-dependent manner electrically evoked contractions in the rat vas deferens. This action was not modified by yohimbine, naloxone or a mixture of antagonists containing atropine, phentolamine, methysergide, burimamide, propranolol and indomethacin, but was markedly potentiated by reducing the Ca2+ concentration of the medium from 2.5 to 1.25 mM and greatly inhibited when increasing the Ca2+ concentration of the medium from 2.5 to 5.0 mM. Clonidine (CLO), but not beta-endorphin (ENDO) was affected similarly to SS by changing the Ca2+ concentration of the medium. The contractile effect of norepinephrine in unstimulated rat vas deferens was not altered by SS. These results were taken as an indication that SS produces its inhibitory action in the rat vas deferens by interacting with specific SS and its receptors presumably located in the cell membranes of adrenergic nerve terminals. The interaction between SS and its receptors may provoke a decreased diffusion of Ca2+ ions into the nerve terminals and/or a decreased mobilisation of Ca2+ ions from intraneuronal stores thus leading to a reduction in electrically evoked release of norepinephrine.
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PMID:Studies on the inhibitory action of somatostatin in the electrically stimulated rat vas deferens. 46 93

Somatostatin and dihydrosomatostatin (H2somatostatin) are equipotent in inhibiting insulin and glucagon release induced by arginine in the rat. The ID50 of H2somatostatin on insulin and glucagon secretion induced by arginine are 14 +/- 6 and 6 +/- 10 mug/100 g BW respectively, similar to the ID50 of H2somatostatin (18 +/- 10 mug/100 g BW) on inhibition of insulin release induced by glucose. Thyrotropin releasing factor, luteinizing hormone releasing factor, alpha-MSH, and the N-terminus decapeptide of the beta-chain of porcine hemoglobin did not alter the secretion of insulin and glucagon induced by arginine. With the exception of [Ala2[-somatostatin and [Ala5]-somatostatin, alanine substituted analogs of somatostatin were less potent than somatostatin. [D-Trp8]-somatostatin is 6-8 times as potent as somatostatin in inhibiting insulin and glucagon release induced by arginine. The relative potencies of these analogs to inhibit the secretion of the pancreatic hormones are in good agreement with our previously reported values based on the inhibition of GH secretion in vitro.
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PMID:Biological activity of somatostatin and somatostatin analogs on inhibtion of arginine-induced insulin and glucagon release in the rat. 81 91

This investigation has been carried out on 50 samples of fetal pancreata from the 10th to the 32nd week of gestation using the PAP technique. beta-Endorphin-reactive cells were morphometrically recorded by means of the point-counting method. beta-Endorphin reactivity occurred for the first time during the 15th week. During further development, beta-endorphin cells were found inside and outside the islets. From the 18th to 23rd week, these cells were primarily localized in the islet periphery. From the 24th week, they rearranged and occurred in irregular positions mixed with other islet cells. This rearrangement took place with a 4 week delay compared with the basic cell types of the islet organ. The extrainsular portion of these cells in the exocrine parenchyma varied between 0.3% in the 27th week and up to 10% in the 22nd week. Concerning the adult human pancreas, it has been suggested whether beta-endorphin cells may be a 6th basic cell type of the islet organ. Previous studies on the coexistence of somatostatin, glucagon and beta-endorphin in the same islet cell and the morphometric analysis would support this assumption. Biochemical examinations indicate that beta-endorphin is a modulator of insulin, glucagon, and somatostatin secretion in the islet organ. This is supported by the fact that beta-endorphin cells have extended cell bodies which is typical of cells with paracrine function.
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PMID:Beta-endorphin-immunoreactive cells in the human fetal pancreas. 128 44

Our previous studies have shown that stimulation of the anteroventral third ventricle region increases atrial natriuretic peptide (ANP) release, whereas lesions of the anteroventral third ventricle or median eminence block the release of ANP from blood volume expansion, suggesting a critical central nervous system participation in this response. ANP is also produced within neurons that have cell bodies in the rostral hypothalamus and axons that extend to the median eminence and neural lobe. In addition to its natriuretic effect, the peptide can inhibit the release of corticotropin (ACTH) and prolactin, anterior pituitary hormones that are released during stress. To determine the physiologic significance of ANP in the control of basal and stress-induced release of anterior pituitary hormones, highly specific antiserum against the peptide (AB-ANP) was microinjected into the third cerebral ventricle of conscious freely moving male rats to immunoneutralize hypothalamic ANP. In the initial experiment, the antiserum or control normal rabbit serum (NRS) was injected into the third cerebral ventricle to determine the effect of the antiserum on basal release of pituitary hormones. The antiserum had no effect on the concentrations of plasma ACTH, prolactin, or thyroid-stimulating hormone for 3 hr after the injection; however, plasma growth hormone concentration, although unchanged for 2 hr, was markedly elevated at 3 hr. These results indicate that although ANP appears to have no effect on the basal release of the other hormones, it has a physiologically significant inhibitory effect on growth hormone release. The delay of the effect is probably related to the time required for the antiserum to diffuse to the site of action of the peptide, presumably at some distance from the ventricle. Since this effect was demonstrable only after 3 hr, in the stress experiment, the antiserum or NRS was microinjected into the third ventricle 3 hr prior to application of ether stress. The rapid elevation of plasma ACTH in NRS-injected rats was markedly augmented by AB-ANP. Ether also induced a rapid increase in plasma prolactin in the NRS-injected animals, as expected. Contrary to the ACTH response, the maximal increase in plasma prolactin after ether was attenuated in animals preinjected with AB-ANP. In the NRS-injected animals, there was a significant decline in plasma growth hormone after the application of ether that was significantly accentuated by AB-ANP, but this was probably the result of the higher initial levels of plasma growth hormone in the ANP-AB group followed by its disappearance with a half-time similar to that of the NRS-injected group. The decline in plasma thyroid-stimulating hormone after ether stress was unaltered in the animals injected with AB-ANP. The results of these immunoneutralization studies suggest that endogenous ANP does not play a role in thyroid-stimulating hormone release. On the other hand, the endogenous peptide appears to have a physiologically significant inhibitory role in suppressing ACTH release during stress, mediated at least partly by suppression of vasopressin release. Endogenous ANP has a pathophysiologic role in augmenting the prolactin release in stress either by inhibiting release of prolactin-inhibiting factors or, alternatively, by enhancing release of prolactin-releasing factors. Endogenous ANP appears to inhibit resting, without altering stress-induced inhibition of growth hormone release by stimulating somatostatin release and/or inhibiting growth hormone-releasing hormone release or by both actions.
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PMID:The role of endogenous atrial natriuretic peptide in resting and stress-induced release of corticotropin, prolactin, growth hormone, and thyroid-stimulating hormone. 133 8

A variety of vasoactive substances including biogenic amines, neuropeptide Y, somatostatin, enkephalin, ACTH, corticotropin-releasing hormone, growth hormone releasing hormone, vasoactive intestinal peptide, calcitonin, and atrial natriuretic factor have been extracted from intra-adrenal and extra-adrenal pheochromocytomas in men. Some of them appear to play an important role for the development of hypertension or clinical serious symptoms. However, informations on the molecular forms of other substances in pheochromocytomas are still limited, and precise amount of the peptides or hormones in the tumors has not yet been quantitated. Numerous in vitro or in vivo studies of this documented neoplasm over the years have been reviewed in this manuscript. Clinical analyses of early diagnosis, localization diagnosis, treatment of multiple endocrine neoplasia, preoperative and operative treatments are also evaluated in this paper. These informations will probably provide additional evidence for the multi-secretory APUD cells of neural crest origin and will contribute the therapy in patients with pheochromocytoma.
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PMID:[Pheochromocytoma--basic and clinical analyses]. 134 92


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