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)

Using immunoperoxidase techniques, the possible localization of pituitary regulatory peptides in fundic, antral and duodenal mucosae was investigated in both rat and man. All results obtained were similar in the two species. No glycopeptide (FSH, LH, TSH) was detected in the digestive tract. With different antisera directed against beta-lipotropin, alpha-MSH, beta-MSH, endorphins, ACTH 1-24, ACTH 17-39, a positive reaction was only obtained in the antral mucosae with an antiserum specific for the synthetic fragment 17-39 of ACTH. However neither the common precursor, proopiomelanocortin, nor the complete sequence of ACTH seem to be present in endocrine cells of the digestive tract. On the other hand, three antisera, directed against human growth hormone (GH), visualized numerous endocrine cells scattered in the glandular epithelium of the fundic and antral mucosae. Most cells were identified as ECL type in the gastric mucosae. Others are probably of the gastrin cell type in the antral mucosa, since these cells could be visualized on adjacent sections either with the antiserum against GH, or with a specific antiserum for gastrin.
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PMID:[Cytologic demonstration of immunoreactivity characteristic of adenopituitary peptides in the digestive epithelium of the rat and man]. 632 84

The acid-producing part of the stomach is rich in peptide-hormone-producing endocrine/paracrine cells of different types. In birds and all mammals studied, ECL cells constitute the quantitatively predominant endocrine cell population in this location. They produce histamine and an as yet unidentified peptide hormone. The paracrine action of the ECL cells is to provide histamine to mediate the stimulating effect of gastrin on the acid-secreting parietal cells: the gastrin-ECL cell-parietal cell axis. Secretion of histamine from the ECL cells was studied in intact conscious rats subjected to gastric submucosal microdialysis and using isolated cells in primary culture. The microdialysis experiments revealed that ECL-cell histamine can be mobilized by the local infusion of gastrin, pituitary adenylate cyclase-activating peptide (PACAP), vasoactive intestinal peptide (VIP), peptide YY (PYY), met-enkephalin, endothelin and noradrenaline/adrenaline. While gastrin and met-enkephalin induced a sustained elevation of the submucosal histamine concentration, endothelin, PYY, PACAP, VIP, and noradrenaline/adrenaline induced a transient elevation. Somatostatin, galanin and the prostanoid, misoprostol, inhibited gastrin-stimulated histamine mobilization. Studies of isolated ECL cells (80-90% purity) showed gastrin, PACAP and VIP to stimulate histamine secretion and somatostatin, galanin and misoprostol to inhibit gastrin-stimulated secretion. At present, it seems unlikely that metenkephalin, endothelin, adrenaline and PYY act directly on the ECL cells in situ since the effects could not be reproduced with isolated ECL cells. Clearly, the ECL cells operate under the multifactorial control of circulating hormones, local hormones, catecholamines, neuropeptides and inflammatory mediators.
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PMID:Control of secretion from rat stomach ECL cells in situ and in primary culture. 1171 81

1. The ECL cells control gastric acid secretion by mobilizing histamine in response to circulating gastrin. In addition, the ECL cells are thought to operate under nervous control and to be influenced by local inflammatory processes. 2. The purpose of the present study was to monitor histamine mobilization from ECL cells in conscious rats in response to locally applied regulatory peptides, candidate neurotransmitters and inflammatory mediators. 3. Microdialysis probes were implanted in the submucosa of the acid-producing part of the rat stomach. Three days later, the agents to be tested were administered via the microdialysis probe and their effects on basal (48 h fast) and stimulated (intravenous infusion of gastrin-17, 3 nmol kg(-1) h(-1)) mobilization of ECL-cell histamine was monitored by continuous measurement of histamine in the perfusate (radioimmunoassay). 4. Locally administered gastrin-17 and sulfated cholecystokinin-8 mobilized histamine as did pituitary adenylate cyclase-activating peptide-27, vasoactive intestinal peptide, peptide YY, met-enkephalin, endothelin and noradrenaline, adrenaline and isoprenaline. 5. While gastrin, sulfated-cholecystokinin-8, met-enkephalin and isoprenaline induced a sustained elevation of the submucosal histamine concentration, endothelin, peptide YY, pituitary adenylate cyclase activating peptide, vasoactive intestinal peptide, noradrenaline and adrenaline induced a transient elevation. 6. Calcitonin gene-related peptide, galanin, somatostatin and the prostanoid misoprostol inhibited gastrin-stimulated histamine mobilization. 7. The gut hormones neurotensin and secretin and the neuropeptides gastrin-releasing peptide, neuropeptide Y and substance P failed to affect ECL-cell histamine mobilization, while motilin and neuromedin U-25 had weak stimulatory effects. Also acetylcholine, carbachol, serotonin and the amino acid neurotransmitters aspartate, gamma-aminobutyric acid, glutamate and glycine were inactive or weakly active as was bradykinin. 8. In summary, a range of circulating hormones, local hormones, catecholamines, neuropeptides and inflammatory mediators participate in controlling the activity of rat stomach ECL cells in situ.
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PMID:ECL-cell histamine mobilization in conscious rats: effects of locally applied regulatory peptides, candidate neurotransmitters and inflammatory mediators. 1173 54