Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Actions of human calcitonin-gene related peptide (hCGRP) on acetylcholine (ACh) discharge and gastrin and somatostatin release from rat antral mucosal-submucosal fragments were examined in both dynamic perifusion experiments and short-term static incubation studies. The principal findings of the dynamic perifusion experiments were that hCGRP exerted a dual or biphasic effect on ACh discharge and gastrin release. Initial exposure of antral tissues to hCGRP (1 x 10(-8) M) resulted in stimulation of both ACh and gastrin release that was of brief duration. Continued hCGRP perifusion caused subsequent inhibition of ACh and gastrin release that was substantially greater in duration and magnitude than the initial stimulatory responses. Static incubation studies indicated that hCGRP (10(-10) to 10(-7) M) stimulated somatostatin and inhibited gastrin release in a dose-dependent manner. Inhibition of gastrin and ACh release by hCGRP appeared to be an indirect effect that was mediated by somatostatin as suggested by studies with pertussis toxin (200 ng/ml). Furthermore, studies with atropine (1 x 10(-6) M) and tetrodotoxin (1 x 10(-6) M) indicated that CGRP-induced stimulation of somatostatin release and inhibition of ACh discharge occurred independent of muscarinic receptor activation and nerve excitation. In conclusion, results of these studies indicate that CGRP is capable of exerting both stimulatory and inhibitory effects on ACh release from mucosal-submucosal neurons and gastrin release from antral mucosal G cells in in vitro studies. These data suggest that the inhibitory effects of CGRP on cholinergic discharge and gastrin release are due to the paracrine effects of somatostatin released from antral D cells by direct action of CGRP.
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PMID:Calcitonin gene-related peptide: mechanisms of modulation of antral endocrine cells and cholinergic neurons. 134 8

Neuropeptides, synthesized in dorsal root ganglia (DRG), are implicated in nociception and neurogenic inflammation. Alterations in DRG neuropeptide levels have been described in polyarthritic rats, but these models are associated with widespread systemic disease. Using mild adjuvant-mediated monoarthritis of the left carpal joint we found significant increases in substance P (+69%) and calcitonin gene-related peptide (CGRP; +204+), but not somatostatin in ipsilateral C6/7 DRG. Peptide levels in contralateral DRG and other ipsilateral DRG were unaltered. Substance P and CGRP in DRG may be of importance in the pathogenesis and maintenance of adjuvant arthritis.
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PMID:Increase in substance P and CGRP, but not somatostatin content of innervating dorsal root ganglia in adjuvant monoarthritis in the rat. 137 70

Calcitonin gene-related peptide is a potent inhibitor of stimulated pancreatic exocrine secretion in vivo. The mechanism of this inhibitory action was studied in dogs and rats. The questions examined were: (1) is the inhibitory action of CGRP on pancreatic secretion mediated by somatostatin? (2) is the inhibition direct, via action on acinar cells, or indirect? and (3) is a neuronal mechanism involved, and, if so, by what pathway? In dogs with chronic pancreatic fistulae, CGRP caused significant inhibition of the outputs of pancreatic protein (63-68%) and of pancreatic bicarbonate (74-89%) and a simultaneous dose-related rise (40-102 fmol/ml) in plasma somatostatin-like immunoreactivity. A similar degree of inhibition was found when exogenous somatostatin was infused to achieve similar levels of plasma somatostatin-like immunoreactivity. More direct evidence of somatostatin mediation of CGRP action was sought in conscious rats with pancreatic fistulae using a potent and specific monoclonal antibody to somatostatin. The latter studies suggest that CGRP has both a somatostatin-dependent and a somatostatin-independent mechanism of action. In isolated rat acini, CGRP did not inhibit CCK-stimulated amylase release, suggesting that its in vivo action is indirect. In the isolated vascularly perfused rat pancreas, CGRP (10(-10)-10(-7) M) inhibited in a dose-dependent manner volume and protein output stimulated by a mixture of CCK-8 and secretin. The inhibitory action of CGRP was blocked by tetrodotoxin (10(-7) M) and by atropine (10(-7) M), but not by hexamethonium (10(-7) M). We conclude that CGRP action: (1) is partly explained by release of somatostatin; (2) is indirect; (3) is neurally mediated; and (4) involves cholinergic muscarinic neurons within the pancreas.
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PMID:Selective release of somatostatin by calcitonin gene-related peptide and influence on pancreatic secretion. 137 16

CGRP, substance P (SP), VIP and somatostatin were demonstrated in the internal gills of larval bullfrogs using the immunohistochemical peroxidase-antiperoxidase method. Three groups of immunoreactive fibers were distinguished by their distribution area. The first group includes CGRP, SP and VIP immunoreactive fibers running in the connective tissue of the gill tufts. These fibers were associated with the capillaries. Some CGRP fibers were distributed similarly to SP fibers, and the density of VIP immunoreactive fibers was low. The second group includes CGRP, SP, VIP and somatostatin fibers distributed in the connective tissue surrounding the ceratobranchialia. The third group includes CGRP, SP and somatostatin fibers located in the branchial muscle. Their terminals appeared to be neuromuscular junctions. No immunoreactivity of leu- or met-enkephalins was found in the internal gills. From these findings, the first group of fibers is presumed to be involved in modulating ion transport of the internal gills. The second group of fibers except for the somatostatin fibers is thought to be continuations of the first group of fibers. The third group of fibers may possibly be involved in the modulation of transmissions at the neuromuscular junction. It is unclear whether somatostatin terminals are also involved in this.
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PMID:Distribution of CGRP, substance P, VIP and somatostatin immunoreactive nerve fibers in the internal gills of larvae of the bullfrog, Rana catesbeiana. 138 6

A central action of CGRP to inhibit gastric acid secretion, demonstrated in rats and dogs, is mediated at least in rats through modulation of parasympathetic outflow to the stomach. The centrally mediated protective effects of CGRP against ethanol-induced lesions is unique to this peptide and not shared by other centrally acting inhibitors of gastric function. It may be related to the increase in gastric mucosal blood flow induced by central CGRP. The presence of CGRP-like immunoreactivity and receptors in medullary nuclei receiving visceral information and influencing vagal outflow suggests a possible role of the peptide in the central regulation of gastric function. Peripheral injection of CGRP is well established to inhibit acid secretion in rats, dogs, rabbits, and humans. Its antisecretory effect is unlikely to be related to a direct action on the parietal cells. It involves specific and marked release of gastric somatostatin through an interaction with CGRP receptors characterized on D cells and coupled with cAMP. In addition, CGRP induces a decrease in acetylcholine transmission in the enteric nervous system, which may contribute to the inhibition of acid. The rich innervation of the stomach with CGRP-like immunoreactivity, which forms the major component of gastric sensory fibers, along with peptide release by sensory stimulation and potent actions on gastric secretions suggests a role of the peptide in the regulation of gastric function.
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PMID:Inhibition of gastric acid secretion and ulcers by calcitonin [correction of calciton] gene-related peptide. 163 88

Pig thyroid glands were surgically isolated in situ and perfused with autologous blood to which was added known concentrations of calcitonin gene-related peptide (alpha CGRP). When thyroids were perfused with measured concentrations of CGRP within the range of 0.6-600 nM, the secretion rate of calcitonin (CT) was stimulated while the release of T3, T4, and somatostatin remained unchanged. Specific binding of 125I-CGRP to pig thyroid plasma membranes was demonstrated, and binding was inhibited by unlabelled CGRP but not by CT or by other peptides unrelated structurally to CGRP. The findings indicate that the pig thyroid gland contains plasma membrane binding sites for CGRP and that CGRP is capable of stimulating the secretion of CT.
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PMID:Stimulation of calcitonin secretion in the pig by calcitonin gene-related peptide. 167 68

In addition to differences between the two submucosal ganglionic neural networks, i.e., the plexus submucosus externus (Schabadasch) and the plexus submucosus internus (Meissner), with respect to the occurrence and distribution of serotonin as neurotransmitter, immunocytochemistry also revealed a distinct distribution for various neuropeptides in these two plexuses. Immunoreactivity for galanin, vasoactive intestinal polypeptide, calcitonin gene-related peptide, substance P, neuromedin U, enkephalin, somatostatin and neuropeptide Y was found in varicose and non-varicose nerve fibres of both submucosal ganglionic plexuses, albeit with a distinct distributional pattern. The difference in neurotransmitter and/or neuromodulator content between both neural networks became even more obvious when attention was focussed on the immunoreactivity of the nerve cell bodies for these substances. Indeed, neuropeptide Y, enkephalin- and somatostatin-immunoreactive neuronal perikarya as well as serotonergic neuronal cell bodies appear solely in the plexus submucosus externus. Neuromedin U-immunoreactive perikarya, mostly coexisting with substance P, are observed in large numbers in the plexus submucosus internus, whilst they are rare in the plexus submucosus externus. Double-labelling immunostaining for substance P with CGRP and galanin revealed a different coexistence pattern for the two submucosal ganglionic plexuses. The differing chemical content of the neuronal populations supports the hypothesis that the existence of the two submucosal ganglionic plexuses, present in most large mammals including man, not only reflects a morphological difference but also points to differentiated functions.
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PMID:Distinct distribution of CGRP-, enkephalin-, galanin-, neuromedin U-, neuropeptide Y-, somatostatin-, substance P-, VIP- and serotonin-containing neurons in the two submucosal ganglionic neural networks of the porcine small intestine. 169 6

Somatostatin-14 (SS-14) and somatostatin-28 (SS-28) produce concentration dependent reductions in short-circuit current in rat colonic mucosa. EC50 values of 15.0 and 13.3 nM were obtained for SS-14 and SS-28 respectively while the N-terminal fragments of SS-28, namely somatostatin-(1-12) (SS1-12) and somatostatin-(1-14) (SS1-14) were inactive. Cyclo(Pro-Phe-D-Trp-Lys-Thr-Phe) and cyclo(Pro-Tyr-D-Trp-Lys-Thr-Phe) were potent antisecretory peptides, like SS-14 and SS-28; while the putative somatostatin antagonist, cyclo(7-aminoheptanoyl-Phe-D-Trp-Lys-Thr[Bzl]) exhibited neither agonist nor antagonist effects. Responses to SS-14 could be regulated by agents which affected the secretory state of the epithelium. Antisecretory effects of SS-14 were markedly attenuated by piroxicam and were restored following piroxicam plus either forskolin or vasoactive intestinal polypeptide (VIP). SS-14 also attenuated secretory responses produced by carbachol, substance P (SP), VIP and alpha- and beta-calcitonin gene related peptide (alpha-, beta-CGRP). Therefore, SS-14 exhibits broad spectrum antisecretory effects in rat descending colon mucosa.
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PMID:The antisecretory effects of somatostatin and analogues in rat descending colon mucosa. 170 67

Immunohistochemical localization of substance P (SP), CGRP, VIP, neuropeptide Y (NPY), and somatostatin (SOM) in the carotid labyrinth were compared in some species of amphibians using the peroxidase-antiperoxidase method. Immunoreactivity of SP, CGRP, VIP, and NPY was found in the nerve fibers distributed in the intervascular stroma of the carotid labyrinth. SP, CGRP, and VIP immunoreactive varicose fibers were densely distributed in the peripheral portion of the carotid labyrinth. Some SP-immunoreactive fibers were distributed similarly to CGRP-immunoreactive fibers. The density of NPY and SOM immunoreactive varicose fibers was low. No immunoreactivity of enkephalins was observed in the labyrinth. The intensities of these peptides were varied from species to species. No glomus cells showed immunoreactivity for any of the 7 peptides studied. These results suggest that the vascular regulatory function, which is one of the possible functions of the carotid labyrinth, is controlled by the peptidergic mechanisms in addition to regulation through intimate apposition of glomus and smooth muscle cells (g-s connection).
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PMID:Localization of substance P, CGRP, VIP, neuropeptide Y, and somatostatin immunoreactive nerve fibers in the carotid labyrinths of some amphibian species. 171 15

We have found vasoactive intestinal polypeptide (VIP)-, neurotensin-, substance P-, gastrin-releasing peptide-, calcitonin-, calcitonin gene related peptide (CGRP-2)-, and somatostatin-like immunoreactivities in extracts of sporadic human parathyroid adenomas (n = 18). The content of CGRP-2, substance P, and somatostatin in adenomas correlated directly with that of parathyroid hormone. In addition, concentrations of VIP versus substance P and somatostatin versus CGRP-2 in adenomas were directly correlated. Neuropeptide content of parathyroid hyperplasias differed from that of adenomas. VIP was detected in only one of seven parathyroid hyperplasias, and neurotensin was undetectable (0/7), whereas substance P was present in six of seven cases and GRP in five of seven hyperplasias. In hyperplasias, content of substance P correlated directly with that of gastrin-releasing peptide. Peroxidase immunohistochemistry localized VIP-like immunoreactivity to 20% to 50% of both chief and oxyphilic cells and rare clear cells and capillary endothelium in 11 of 12 adenomas studied. Focal staining was present in glandular epithelium of the rim of adjacent normal parathyroid tissue and in two of three normal parathyroid glands removed with thyroid goiters. This staining was both cytoplasmic and apical membrane. By contrast, in adenomas, neurotensin- and substance P-like positivities were confined to scattered (5% to 10%) oxyphilic cells. Cytoplasmic positivity for parathyroid hormone, noted in 30% to 70% of cells in serial sections, confirmed that these tissues were indeed parathyroid glands.
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PMID:Vasoactive intestinal polypeptide-, neurotensin-, substance P-, gastrin-releasing peptide-, calcitonin-, calcitonin gene related peptide-, and somatostatin-like immunoreactivities in human parathyroid glands. 172 Sep 2


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