PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 21369495-11 2011 The stimulating effect of CCK-8 was significantly inhibited by an anti-PYY serum, and was completely abolished by loxiglumide, and almost completely abolished by atropine. Atropine 162-170 cholecystokinin Rattus norvegicus 26-29 23499805-10 2013 Atropine decreased sensitivity to CCK-8. Atropine 0-8 cholecystokinin Rattus norvegicus 34-37 11298994-7 2001 The increased responsiveness of jejunal motility to CCK persisted after mast cell stabilisation or depletion but was prevented by atropine, devazepide and L-365260 (CCK-A and CCK-B receptor antagonists, respectively) and vagotomy. Atropine 130-138 cholecystokinin Rattus norvegicus 52-55 11257316-5 2001 CART peptide-induced increases in pancreatic secretion appear to involve pathways that are sensitive to both acetylcholine (ACh) and cholecystokinin (CCK) since pre-treatment with atropine (ACh receptor antagonist) or L-364,718 (CCK-A receptor antagonist) inhibited the effects of CART peptide on amylase secretion. Atropine 180-188 cholecystokinin Rattus norvegicus 150-153 9138250-7 1997 The CCK release produced by luminal sodium oleate was inhibited by atropine, but not affected by EABI. Atropine 67-75 cholecystokinin Rattus norvegicus 4-7 9887006-0 1999 Atropine-resistant secretion of a putative luminal CCK-releasing peptide in conscious rats. Atropine 0-8 cholecystokinin Rattus norvegicus 51-54 10427693-3 1999 In this study, we found that guanidinated casein hydrolysate stimulates CCK release in chronic BPJ-diverted rats with cholinergic control blocked by atropine. Atropine 149-157 cholecystokinin Rattus norvegicus 72-75 10427693-4 1999 Intraduodenal guanidinated casein hydrolysate increased portal plasma CCK concentration and pancreatic secretion in atropine-treated BPJ-diverted rats. Atropine 116-124 cholecystokinin Rattus norvegicus 70-73 8779966-5 1996 The vasodilator response to low-dose CCK-8 (0.04 nmol/min) was further analyzed and found to be inhibited by acute bilateral subdiaphragmatic vagotomy, atropine (1 mumol/kg ip), and the antagonistic calcitonin gene-related peptide (CGRP) fragment CGRP-(8-37) (6 nmol/ min ia). Atropine 152-160 cholecystokinin Rattus norvegicus 37-40 8843776-5 1996 The CCK-independent increases by HGC instillation are completely depressed by atropine. Atropine 78-86 cholecystokinin Rattus norvegicus 4-7 8843776-8 1996 We conclude that the stimulatory effects of dietary protein on the pancreatic enzyme secretion partially do not depend on CCK in chronic BPJ-diverted rats and that the CCK-independent increase is atropine sensitive. Atropine 196-204 cholecystokinin Rattus norvegicus 168-171 8795088-8 1996 In this study, 2 ng of oxytocin decreased plasma levels of CCK, gastrin and somatostatin, effects that were blocked by pretreatment with atropine. Atropine 137-145 cholecystokinin Rattus norvegicus 59-62 8100836-5 1993 Pretreatment with atropine or hexamethonium completely abolished pancreatic protein response to low doses of CCK-8 (10-40 pmol/kg per h) but had only partial effect on doses > 40 pmol/kg per h. Bilateral vagotomy also abolished the pancreatic responses to low doses of CCK-8. Atropine 18-26 cholecystokinin Rattus norvegicus 109-112 7959408-6 1994 The potentiation of the acid secretory response to CCK-8 by the CCKA antagonist was completely blocked by vagotomy or atropine, as well as hexamethonium. Atropine 118-126 cholecystokinin Rattus norvegicus 51-54 8100836-5 1993 Pretreatment with atropine or hexamethonium completely abolished pancreatic protein response to low doses of CCK-8 (10-40 pmol/kg per h) but had only partial effect on doses > 40 pmol/kg per h. Bilateral vagotomy also abolished the pancreatic responses to low doses of CCK-8. Atropine 18-26 cholecystokinin Rattus norvegicus 272-275 2281081-4 1990 Intestinal secretion as a source of the putative trypsin-sensitive intestinal CCK-releasing peptide was obtained by rapid intestinal perfusion of isolated Thiry-Vella fistulae of jejunum in conscious rats, collected with or without atropine pretreatment. Atropine 232-240 cholecystokinin Rattus norvegicus 78-81 1683164-7 1991 Atropine (50 micrograms.kg-1.h-1) did not affect the incremental responses to low doses of CCK-8; the maximal response occurred at a higher CCK-8 dose because atropine decreased basal secretion. Atropine 159-167 cholecystokinin Rattus norvegicus 140-143 1683164-9 1991 We conclude that 1) bethanechol is a full agonist for stimulation of pancreatic enzyme secretion and its effects are not mediated by CCK release; 2) atropine is a competitive antagonist of bethanechol-induced pancreatic secretion in vivo but does not directly affect responses to CCK-8; 3) cholinergic mechanisms do not mediate the pancreatic enzyme response to a liquid meal in rats. Atropine 149-157 cholecystokinin Rattus norvegicus 280-283 1719526-5 1991 The incremental pancreatic secretion, including juice volume and amylase output, in response to intravenous infusion of CCK-8 with secretin, was significantly suppressed by intravenous administration of atropine in a dose of 100 micrograms/kg/h (p less than 0.01). Atropine 203-211 cholecystokinin Rattus norvegicus 120-123 2235972-0 1990 Atropine enhances food-stimulated CCK secretion in the rat. Atropine 0-8 cholecystokinin Rattus norvegicus 34-37 2235972-9 1990 Plasma CCK 15 min after beginning the diet infusion was significantly increased by atropine (8.09 +/- 1.77 pM in atropine-treated rats versus 3.14 +/- 0.64 pM in controls). Atropine 83-91 cholecystokinin Rattus norvegicus 7-10 2235972-9 1990 Plasma CCK 15 min after beginning the diet infusion was significantly increased by atropine (8.09 +/- 1.77 pM in atropine-treated rats versus 3.14 +/- 0.64 pM in controls). Atropine 113-121 cholecystokinin Rattus norvegicus 7-10 2473503-6 1989 The stimulated CCK plasma levels were significantly lowered by the infusion of atropine 60 min, but not 180 min, after feeding of camostate. Atropine 79-87 cholecystokinin Rattus norvegicus 15-18 2466220-3 1989 CCK-8 produced a saturable and potent (EC50 = 3 nM) facilitation of KCl (35 mM)-evoked [3H]DA efflux from nucleus accumbens, but failed to significantly alter [3H]DA efflux from striatum: The stimulatory action of CCK-8 was unaffected by the muscarinic antagonist atropine, the opiate antagonist naloxone, or the selective ion channel blockers tetrodotoxin and nifedipine. Atropine 264-272 cholecystokinin Rattus norvegicus 0-3 6713495-5 1984 When the antagonist atropine was applied after carbachol stimulation, deposits reappeared on cell membranes, which then disappeared again after a second stimulation with cholecystokinin. Atropine 20-28 cholecystokinin Rattus norvegicus 170-185 6299117-5 1983 Phentolamine, phenoxybenzamine, propranolol, catecholamine depletion of preparations by reserpine-tetrabenazine, and the block of catecholamine synthesis at different levels significantly inhibited CCK-OP-induced tonic contraction, whereas atropine had no influence. Atropine 240-248 cholecystokinin Rattus norvegicus 198-201 3953805-9 1986 Intraduodenal perfusion of lidocaine, infusion of tetrodotoxin into the superior mesenteric artery, or intravenous infusion of atropine inhibited the rise in plasma cholecystokinin seen with diversion of pancreaticobiliary juice. Atropine 127-135 cholecystokinin Rattus norvegicus 165-180 7223893-6 1981 In the presence of 2 mmol/l La3+, the atropine-induced 45Ca2+ uptake in CCh-pretreated cells and the dibutyryl guanosine 3",5"-cyclic monophosphate-induced 45Ca2+ uptake in CCK-OP-pretreated cells were highly reduced. Atropine 38-46 cholecystokinin Rattus norvegicus 173-176 6893892-13 1980 It was concluded that atropine had a complex effect on pancreatic secretion: it possibly decreased the CCK release in the first period after diversion but not later, and decreased the duodenopancreatic reflexes and other factors of the cholinergic tone. Atropine 22-30 cholecystokinin Rattus norvegicus 103-106