Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT02427 (Atropine)
 3,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intracellular microelectrode and standard organ bath techniques were used to study in vitro the effects of three molecular forms of the peptide cholecystokinin on the electrical and mechanical activities of canine antral circular muscle. Three forms were studied: the carboxyl-terminal octapeptide of cholecystokinin (CCK-OP), the molecule containing 33 amino acid residues (CCK33), and the peptide termed "cholecystokinin variant" that contains 39 amino acids (CCK39). All three forms increased the force and frequency of spontaneous contractions. They also increased the frequency and the amplitude and duration of the plateau of the gastric action potential. Atropine did not block any of these effects, suggesting that the action of these peptides was largely due to a direct action on the smooth muscle. Complete dose-response curves were determined for the effect of these peptides on the force and frequency of contraction for muscle strips and for the effect on amplitude of the plateau and frequency of the action potential for single cells. CCK39 and CCK-OP had similar potencies and both forms were more potent than CCK33.
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PMID:Electrical and mechanical effects of molecular variants of CCK on antral smooth muscle. 69 26

To explore the interactions between cholecystokinin (CCK) and the cholinergic system, we compared the effect of cholinergic or peptidergic CCK blockade on gallbladder contraction and pancreatic enzyme secretion using atropine and loxiglumide (a specific CCK antagonist) as pharmacological tools. Gallbladder contraction was measured by sonography and pancreatic secretion by a marker perfusion and aspiration technique. Graded doses of exogenous CCK8 induced dose-dependent contractions of the gallbladder and increasing enzyme outputs. Loxiglumide (10 mg kg-1 h-1) abolished the gallbladder response and prevented an increase in pancreatic enzyme secretion to CCK8. Atropine (5 micrograms kg-1 h-1), however, only reduced gallbladder contraction and enzyme output to CCK8. Gallbladder volumes decreased maximally to 12 +/- 4% after oral food, whereas enzyme output and plasma CCK levels increased 6- to 8-fold. Loxiglumide completely abolished gallbladder contraction and inhibited enzyme secretion by 30%. Atropine caused a small reduction in gallbladder volumes, but essentially blocked postprandial enzyme secretion. The results indicate that CCK is the major regulator of gallbladder contraction with the cholinergic system modulating the response, while the exocrine pancreas is crucially dependent on a cholinergic background with CCK modulating the secretory response.
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PMID:Postprandial control of gallbladder contraction and exocrine pancreatic secretion in man. 128 65

The effects of galanin and its interaction with cholecystokinin and acetylcholine on smooth muscle cells were studied in vitro on isolated cells obtained from pig ileum circular muscle layer. Galanin induced a concentration-dependent cell contraction with a maximal contraction (24.5% decrease in cell length from control) obtained at 1 nM. The concentration of galanin inducing a half-maximal contraction was 3 pM. Tetrodotoxin (10 microM) failed to inhibit cell contraction induced by galanin (1 nM), pentagastrin (10 nM) and acetylcholine (1 microM). Atropine abolished the contraction induced by acetylcholine (1 microM), but had no effect on galanin- and pentagastrin-induced contraction. L 364,718 inhibited the contraction induced by CCK8 but not the galanin-induced contraction. At the uneffective concentration of 10 fM, galanin had a synergistic effect with an uneffective concentration of CCK8 (1 pM). These results suggest that (i) galanin contracts smooth muscle cells from pig ileum by acting on a specific receptor; (ii) galanin and either CCK or acetylcholine may act in a synergistic way to induce cell contraction.
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PMID:Galanin induces contraction of isolated cells from circular muscle layer of pig ileum. 171 85

Studies were made on the mode of action of cholecystokinin octapeptide (CCK8) on longitudinal muscle strips of guinea pig ileum in vitro. CCK8 produced dose-related contractions of innervated strips of ileum longitudinal muscle (EC50 3--4 x 10(-9) M), but was inactive on denervated strips. Tetrodotoxin, and reducing the bath temperature to 15 degree C, abolished the response of innervated strips to CCK8. These results indicate that the action of CCK8 on ileal longitudinal muscle is mediated by the myenteric plexus. Atropine abolished the responses to acetylcholine and to low doses of CCK8. However, the responses to CCK8 in doses above 10(-8) M were reduced by atropine but not abolished. Incubation of longitudinal muscle strips with high concentrations of substance P (1.5 x 10(-7) M) resulted in desensitization to this peptide; this treatment inhibited the responses to CCK8 alone, and abolished the atropine-resistant actions of CCK8. Desensitization to substance P had no effect on the responses to acetylcholine, histamine, serotonin and angiotensin II. The results indicate that CCK8 contracts the longitudinal muscle of guinea pig ileum by releasing acetylcholine and substance P from the myenteric plexus.
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PMID:Evidence that the action of cholecystokinin octapeptide on the guinea pig ileum longitudinal muscle is mediated in part by substance P release from the myenteric plexus. 616 53

To determine the role of cholinergic reflexes on pancreatic secretory response to food, we studied the effect of atropine on amylase secretion in response to the octapeptide of cholecystokinin (CCK8) and to intraintestinal oleate. Four studies were done in six healthy volunteers. The duodenal content was aspirated by a double lumen tube while synthetic secretin (41 pmol/kg/h) was infused as a background in all the studies. Graded doses of CCK8 IV or 0.42 M oleate pH 9.4 at 25 ml/h into the intestine with and without atropine 1.8 mg were given on different days. CCK-like immunoreactivity (LI) in the plasma was measured by RIA during the intraintestinal oleate studies. CCK8 stimulated pancreatic enzyme secretion in a dose related fashion, an effect that was not modified by atropine. Intraintestinal oleate also stimulated pancreatic secretion and increased the CCK-LI in the plasma. Atropine significantly (p less than 0.05) decreased the pancreatic enzyme secretion before and during intraintestinal oleate, without effect on the CCK-LI levels. We conclude: (1) that the effect of exogenous CCK on pancreatic secretion of enzymes is not affected by atropine; (2) intraintestinal oleate stimulates pancreatic enzyme secretion significantly by an atropine-sensitive mechanism; (3) probably the atropine effect is a blockade of a cholinergic enteropancreatic reflex.
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PMID:Cholinergic component in the human pancreatic secretory response to intraintestinal oleate. 619 36

In this study, we describe new methods for recording gastric emptying and in vivo measurements of intragastric pressure in fish. Using these methods, we investigated the effects of the sulphated octapeptide of cholecystokinin (CCK8) on gastric emptying and on stomach motility in vivo and in vitro. Gastric emptying of 99Tcm-labelled food was measured in swimming fish by using a gamma camera, counting consecutive 2.5 min periods for 18-42 h. After 20 h, 55.3+/-4.0 % of the labelled food remained in the stomach of the control fish (mean s.e.m., N=9). Vascular infusion of CCK8 (25 pmol kg-1 h-1) delayed gastric emptying so that 70.4+/-4.8 % of the labelled food remained in the stomach after 20 h (N=8). Gastric pressure changes in vivo were measured using a balloon surgically fitted into the cardiac or pyloric part of the stomach. In the cardiac part, intra-arterial infusion of CCK8 at 0.1 nmol kg-1 h-1 resulted in a decrease in the frequency and amplitude of rhythmic contractions, while higher doses started/increased contractions. Atropine blocked much of the basal contractile activity, but did not influence the CCK8-induced inhibition of contractile activity. The pyloric part of the stomach was unaffected by intra-arterial infusion of CCK8 or atropine. In vitro perfusion of the stomach (with a balloon placed in the cardiac part to record motility) with CCK8 at high concentrations (10(-7 )mol l-1 and above) augmented the spontaneous contractions, while lower concentrations had inconsistent effects. In addition, CCK8 (10(-7) to 10(-6 )mol l-1) decreased the amplitude of spontaneous contractions in longitudinal strip preparations, usually in combination with an increase in the resting tension. The decrease in amplitude was not affected by the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester hydrochloride (L-NAME; 10(-4 )mol l-1). Depending on the concentration and experimental arrangement, CCK8 had either inhibitory or excitatory effects on the cardiac stomach, suggesting the possible presence of different types of CCK receptor. We conclude that the predominant effect of CCK8 in vivo may be a slowing down of gastric emptying, presumably coinciding with a release of bile into the duodenum.
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PMID:Cholecystokinin affects gastric emptying and stomach motility in the rainbow trout Oncorhynchus mykiss. 985 5