Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Based upon the findings in over 1200 patients, technique, indication and validity of pharmacoradiology in examinations of esophagus, stomach, duodenum, small and large intestine are critically evaluated and summarized. Dosis, effects, side effects and contraindications of the mostly applied pharmaca (Buscopan, Pro-Banthine, Paspertin, Glucagon, Cholecystokinin and Caerulein) are listed. The value of pharmacoradiology of the gastrointestinal tract for clinical roentgenology is stressed.
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PMID:[Present status of pharmacoradiology of the gastrointestinal tract (author's transl)]. 101 16

The inhibition of the pentagastrin-stimulated (1 ug/kg b.w./hour) gastric secretion by glucagon (20 ug/kg b.w./hour), cholecystokinin (0.5 IDU/kg b.w./hour), and a combination of these were investigated in 7 volunteers. Glucagon as well as CCK given isolated inhibited the gastric secretion, but no augmentation of inhibition was demonstrated when the hormones were in combination.
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PMID:Combined effect of glucagon and cholecystokinin on gastric secretion in man. 106 39

A specific radioimmunoassay for motilin has been developed with the use of antisera to porcine motilin raised in guinea pigs. Highly purified 125-I-motilin was used as the tracer and the sensitivity range was 10 to 320 pg. No cross-reactivity was demonstrated with gastric inhibitory polypeptide, secretin, glucagon, gastrin, cholecystokinin-pancreozymin, or vasoactive intestinal peptide. In dogs with denervated pouches of the fundus of the stomach and Mann-Bollman fistulae, duodenal alkalinization resulted in an increase in gastric motor activity in the fundic pouch with a corresponding increase in serum motilin.
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PMID:Radioimmunoassay for motilin. 112 96

COOH-terminal octapeptide of cholecystokinin (CCK-octapeptide) and the cholinergic agent carbamylcholine each produced a fourfold stimulation of calcium outflux in guinea pig isolated pancreatic acinar cells. Neither agent altered calcium influx. Stimulation of calcium outflux was rapid and specific, was abolished by reducing the incubation temperature to 4 degrees C, and was a saturable function of the secretagogue concentration. The concentrations of CCK-octapeptide and carbamylcholine that produced half-maximal stimulation of calcium outflux were 3.1 x 10(-10) M and 4.9 x 10(-5) M, respectively. The cholinergic antagonist antropine competitively inhibited carbamylcholine stimulation of calcium outflux but did not alter stimulation produced by CCK-octapeptide. Stimulation of calcium outflux by maximal concentrations of carbamycholine plus CCK-octapeptide was the same as that produced by a maximal concentration of either agent alone.Calcium outflux became refractory to stimulation by secretagogues, and incubation with either CCK-ostapeptide or carbamylcholine produced a refractoriness to both agents. The relative potencies with CCK and its related fragments stimulated calcium outflux were CCK-octapeptide greater than heptapeptide greater than CCK greater than hexapeptide = gastrin. Secretin, glucagon, and vasoactive intestinal peptide, at concentrations as high as 10(-5) M, failed to alter calcium outflux and did not affect stimulation by CCK-octapeptide or by carbamycholine.
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PMID:Action of cholecystokinin and cholinergic agents on calcium transport in isolated pancreatic acinar cells. 115 Aug 77

The vasoactive effects of cholecystokinin-octapeptide (CCK-OP), pentagastrin, synthetic secretin, glucagon, and acetylcholine were assessed in the intestinal circulation of the dog. In pharmacologic doses of glucagon, CCK-OP, and, to a lesser degree, pentagastrin significantly increased blood flow and oxygen consumption. Atropine blocked the vasodilator effects of CCK-OP, pentagastrin, and acetylcholine but did not block those of glucagon. Neither the alpha-adrenergic blocker, phenoxybenzamine, nor the beta-adrenergic blocker, propranolol, blocked the vasodilator response to pentagastrin. Synthetic secretin had no significant effect on either blood flow or oxygen consumption in the intestinal segment. The vasodilator response to CCK-OP and pentagastrin appears to be mediated specifically through cholinergic receptors.
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PMID:Pharmacologic effects of gastrointestinal hormones on intestinal oxygen consumption and blood flow. 116 16

The effects of intravenous infusion of synthetic C-terminal octapeptide of cholecystokinin (OP-CCK) on concentrations of insulin and glucagon in peripheral venous plasma of conscious dogs were studied. Both hormones increased in response to 160 and 480 ng/kg/h of OP-CCK. The increases to 480 ng/kg/h were larger than those to 160 ng/kg/h. Peripheral venous concentrations of glucose and intestinal glucagon-like immunoreactivity were not altered by OP-CCK. OP-CCK, 160 ng/kg/h, did not enhance insulin and glucagon responses to intravenous infusion of amino acids. The results suggest that insulin- and glucagon-releasing actions of porcine cholecystokinin preparations should not be attributed entirely to gastric inhibtory polypeptide or other impurities contained in these preparations since the synthetic active fragment of cholecystokinin alone increases insulin and and glucagon concentrations in peripheral plasma.
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PMID:Effects of the octapeptide of cholecystokinin on insulin and glucagon secretion in the dog. 117 6

The morphology and distribution of secretin (S) cells were investigated in the human and the dog. S cells were well-visualized by the indired immunofluorescence antibody technique, using a highly specific rabbit anti-secretin sera. The fluorescence reaction was not blocked by an excess amount of gastrin, cholecystokinin, glucagon, vasoactive intestinal polypeptide, or motilin, whereas secretin blocked the reaction. S cells were seen in the mucosa of the antrum and duodenum in both humans and dogs, and throughout the entire length of the canine small intestine. They were not found in the mucosa of the esophagus, fundus of the stomach, or rectum. These cells were either pyramidal in shape or pearshaped and were one-third of the size of gastrin cells. The possible significance of S-cell distribution in the antrum and small intestine is discussed.
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PMID:Secretion cells in the gastrointestinal tract. 127 7

Dogs were given a prostaglandin analogue, misoprostol, at a dose that significantly increases gastrointestinal epithelial cell proliferation. Both basal and postprandial concentrations of gastrin were significantly higher in the misoprostol-treated dogs and more than doubled after the meal in both the controls and in the test group. Plasma enteroglucagon, cholecystokinin, insulin and glucose-dependent insulinotrophic peptide all increased postprandially, with no effect of misoprostol. Tissue concentrations of bombesin, gastrin and somatostatin were unaffected by misoprostol, but the fundic glucagon-like immunoreactivity was significantly increased. Thus high doses of misoprostol have only minor effects on gastrointestinal regulatory peptides, suggesting that the trophic effect of prostaglandins on the intestinal tract may be direct.
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PMID:Plasma and tissue hormones in the dog after administration of the prostaglandin analogue, misoprostol. 128 66

To find mammalian analogues of exendin-4, a peptide from Helodermatidae venoms that interacts with newly discovered exendin receptors on dispersed acini from guinea pig pancreas, we examined the actions of recent additions to the vasoactive intestinal peptide/secretin/glucagon family of regulatory peptides. In every respect tested, the truncated form of glucagon-like peptide-1, GLP-1(7-36)NH2, mimicked the actions of exendin-4. Like exendin-4, GLP-1(7-36)NH2 caused an increase in acinar cAMP without stimulating amylase release. GLP-1(7-36)NH2-induced increases in cAMP were inhibited progressively by increasing concentrations of the specific exendin-receptor antagonist, exendin(9-39)NH2. In dispersed acini from guinea pig and rat pancreas, concentrations of GLP-1(7-36)NH2 that stimulated increases in cAMP caused potentiation of cholecystokinin-induced amylase release. Binding of 125I-[Y39]exendin-4 or 125I-GLP-1(7-36)NH2 to dispersed acini from guinea pig pancreas was inhibited by adding increasing concentrations of unlabeled exendin-4 or GLP-1(7-36)NH2. We conclude that the mammalian peptide GLP-1(7-36)NH2 interacts with exendin receptors on dispersed acini from guinea pig pancreas. Exendin(9-39)NH2, a competitive antagonist of the actions of GLP-1(7-36)NH2 in pancreatic acini, may be a useful tool for examining the physiological actions of this peptide.
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PMID:Truncated glucagon-like peptide-1 interacts with exendin receptors on dispersed acini from guinea pig pancreas. Identification of a mammalian analogue of the reptilian peptide exendin-4. 132 31

Many studies suggest that smooth muscle relaxation caused by beta-adrenergic agents and various neuropeptides occurs as a result of an increase in cellular adenosine 3',5'-cyclic monophosphate (cAMP). However, the evidence is indirect, and furthermore does not demonstrate that an increase in cAMP is essential for mediating relaxation. To define more clearly the role of cAMP in receptor-mediated smooth muscle relaxation, we used a specific competitive antagonist of the action of cAMP on protein kinase A, (R)-p-adenosine 3',5'-cyclic phosphorothioate [(R)-p-cAMPS], and its S isomer, (S)-p-cAMPS, which functions as a cAMP agonist. In gastric smooth muscle cells from guinea pig, (S)-p-cAMPS caused a dose-related relaxation [50% inhibitory concentration (IC50) 86 +/- 59 nM]. Vasoactive intestinal peptide (VIP) produced smooth muscle cell relaxation (IC50 2.3 +/- 0.8 nM) through occupation of specific VIP receptors. (R)-p-cAMPS inhibited VIP-induced relaxation, with a rightward shift in the VIP dose-response curve, suggesting competitive antagonism. Furthermore, (R)-p-cAMPS inhibited relaxation induced by other agents that increase cellular cAMP (isoproterenol, calcitonin gene-related peptide, and glucagon) but not that induced by ATP or sodium nitroprusside. (R)-p-cAMPS had no effect on contraction stimulated by carbachol, cholecystokinin, or substance P. These data demonstrate that activation of protein kinase A is primarily responsible for mediating gastrin smooth muscle relaxation produced by adrenergic agents and various neuropeptides.
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PMID:A primary role for protein kinase A in smooth muscle relaxation induced by adrenergic agonists and neuropeptides. 132 27


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