PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18555802-9 2008 CONCLUSIONS: CCK at physiologic concentrations in the presence of atropine and tetrodotoxin elicits cytosolic Ca(2+) signaling, activates mitochondrial function, and stimulates enzyme secretion in isolated human pancreatic acinar cells. Atropine 66-74 cholecystokinin Homo sapiens 13-16 20852067-9 2010 PSCs express ACh synthesizing enzyme, VAChT, synaptophysin, and CCK receptors; exhibit CCK-dependent ACh secretion; and stimulate amylase secretion by acini, which is blocked by atropine. Atropine 178-186 cholecystokinin Homo sapiens 64-67 20852067-9 2010 PSCs express ACh synthesizing enzyme, VAChT, synaptophysin, and CCK receptors; exhibit CCK-dependent ACh secretion; and stimulate amylase secretion by acini, which is blocked by atropine. Atropine 178-186 cholecystokinin Homo sapiens 87-90 12754388-5 2001 It has been clearly shown that PPsecretion is under vagal cholinergic control since thePP response to a meal or CCK infusion is bluntedduring vagal cholinergic blockade with atropine orfollowing truncal vagotomy (1,6). Atropine 174-182 cholecystokinin Homo sapiens 112-115 18248661-11 2008 Blocking CCK(1) or muscarinic receptors completely abolished PHA-stimulated gallbladder contraction (dexloxiglumide 208.7 +/- 23.7%; atropine 104 +/- 7.0% of basal volume) while none of the treatments affected CCK levels. Atropine 133-141 cholecystokinin Homo sapiens 9-12 16718754-10 2006 In addition, intravenous administration of CCK has been observed to reproduce the symptoms in FD and this effect can be blocked both by atropine and loxiglumide (CCK-A antagonist). Atropine 136-144 cholecystokinin Homo sapiens 43-46 7701255-8 1995 A further significant (P = 0.002) increase in the inhibitor-induced CCK output was found during atropine administration, as compared with the test situation without atropine. Atropine 96-104 cholecystokinin Homo sapiens 68-71 14518292-9 1998 Atropine suppressed the low dose CCK effect completely. Atropine 0-8 cholecystokinin Homo sapiens 33-36 14518292-10 1998 Whereas CCK at high doses caused a 1.5 fold increase despite atropine. Atropine 61-69 cholecystokinin Homo sapiens 8-11 9009112-5 1997 Atropine significantly reduced whole colon (change from fasting = 52 +/- 11%) and left colon (change from fasting 61 +/- 8%) phasic pressure activity and transverse colon tone (change from fasting 159 +/- 40%); CCK-OP had no significant effects on phasic contractility, tone or transit. Atropine 0-8 cholecystokinin Homo sapiens 211-214 9136850-7 1997 Thus, this inhibitory effect on gallbladder contraction depended on the hydrophobicity of bile salts and was also specific for certain stimuli such as CCK and field stimulation (mediated by cholinergic nerves, being abolished by atropine and tetrodotoxin). Atropine 229-237 cholecystokinin Homo sapiens 151-154 8582185-1 1995 In the present study, we adopted real-time ultrasonography to investigate the effect of atropine on the gallbladder emptying induced by CCK-OP in the normal subjects, and the difference of gallbladder emptying induced by CCK-OP between the "silent" gallstone patients and the controls. Atropine 88-96 cholecystokinin Homo sapiens 136-139 8582185-2 1995 The results showed that: (a) CCK-induced gallbladder emptying in normal subjects was inhibited from 88.7% +/- 5.5% without atropine to 43.4% +/- 9.4% with atropine (P < 0.001). Atropine 123-131 cholecystokinin Homo sapiens 29-32 8582185-2 1995 The results showed that: (a) CCK-induced gallbladder emptying in normal subjects was inhibited from 88.7% +/- 5.5% without atropine to 43.4% +/- 9.4% with atropine (P < 0.001). Atropine 155-163 cholecystokinin Homo sapiens 29-32 7701255-8 1995 A further significant (P = 0.002) increase in the inhibitor-induced CCK output was found during atropine administration, as compared with the test situation without atropine. Atropine 165-173 cholecystokinin Homo sapiens 68-71 7701255-10 1995 The increase in plasma CCK levels indicates that CCK is feedback-regulated by both an inhibitor-mediated decrease in duodenal enzyme activity and a further decrease in pancreatic enzyme secretion by atropine. Atropine 199-207 cholecystokinin Homo sapiens 23-26 7701255-10 1995 The increase in plasma CCK levels indicates that CCK is feedback-regulated by both an inhibitor-mediated decrease in duodenal enzyme activity and a further decrease in pancreatic enzyme secretion by atropine. Atropine 199-207 cholecystokinin Homo sapiens 49-52 8185159-10 1994 On the other hand, atropine abolished the postprandial increase in pancreatic secretion and in addition markedly reduced the increase in pancreatic secretion due to infusion of "physiological" doses of CCK (i.e., CCK doses that mimic its postprandial increase in plasma). Atropine 19-27 cholecystokinin Homo sapiens 202-205 8185159-10 1994 On the other hand, atropine abolished the postprandial increase in pancreatic secretion and in addition markedly reduced the increase in pancreatic secretion due to infusion of "physiological" doses of CCK (i.e., CCK doses that mimic its postprandial increase in plasma). Atropine 19-27 cholecystokinin Homo sapiens 213-216 1701910-4 1990 Additions of the antagonists N2,O2-dibutyrylguanosine 3":5"-cyclic monophosphate and atropine after 30 min of CCK-8 and carbachol stimulation, respectively, were associated with prompt lowerings of Ca2+i and inhibitions of amylase secretion. Atropine 85-93 cholecystokinin Homo sapiens 110-113 1636705-3 1992 Atropine inhibited CCK-8 (10 ng.kg-1.h-1)-stimulated trypsin output by 84.0 +/- 7.7% and lipase output by 78.6 +/- 9.2%. Atropine 0-8 cholecystokinin Homo sapiens 19-22 1636705-4 1992 The inhibition with atropine was much less with a CCK-8 dose of 40 ng.kg-1.h-1 (41.8 +/- 6.6% for trypsin and 46.3 +/- 7.3% for lipase). Atropine 20-28 cholecystokinin Homo sapiens 50-53 8236019-9 1993 Tetrodotoxin (1 mumol/L) and atropine (1 mumol/L) caused a rightward shift of the dose-response curve for CCK-8-stimulated sphincter relaxation. Atropine 29-37 cholecystokinin Homo sapiens 106-109 1702077-6 1991 The enzyme response to graded doses of exogenous CCK was significantly inhibited by atropine and loxiglumide. Atropine 84-92 cholecystokinin Homo sapiens 49-52 2281081-8 1990 CCK-releasing activity manifested by pancreatic protein secretion was equivalent in intestinal washes from atropine-treated and control Thiry-Vella fistula donor rats. Atropine 107-115 cholecystokinin Homo sapiens 0-3 3803143-4 1987 The total CCK released above baseline was greatest with the infusion of amino acids with atropine, while the total trypsin output above baseline was greatest with the infusion of amino acids. Atropine 89-97 cholecystokinin Homo sapiens 10-13 2282997-0 1990 Cholecystokinin release by gastric distension--an atropine-sensitive mechanism. Atropine 50-58 cholecystokinin Homo sapiens 0-15 2282997-7 1990 Atropine completely blocked PP release and almost abolished CCK release, whereas gastrin output was enhanced. Atropine 0-8 cholecystokinin Homo sapiens 60-63 2282997-10 1990 In conclusion, we demonstrated a gastric phase of CCK release which is atropine sensitive, but not influenced by propranolol. Atropine 71-79 cholecystokinin Homo sapiens 50-53 2373273-0 1990 Inhibition of cholecystokinin-induced gallbladder contraction by atropine and pirenzepine in man. Atropine 65-73 cholecystokinin Homo sapiens 14-29 2683738-4 1989 Atropine (500 micrograms, im) inhibited significantly (p less than 0.01) the gallbladder contraction (maximum contractile rate, 78.7 +/- 6.4%) in response to bombesin without any change of plasma CCK secretion, whereas proglumide (800 mg/day for 3 days, per os) decreased slightly but not significantly the gallbladder contraction, and had no effect on plasma CCK secretion. Atropine 0-8 cholecystokinin Homo sapiens 196-199 2683738-4 1989 Atropine (500 micrograms, im) inhibited significantly (p less than 0.01) the gallbladder contraction (maximum contractile rate, 78.7 +/- 6.4%) in response to bombesin without any change of plasma CCK secretion, whereas proglumide (800 mg/day for 3 days, per os) decreased slightly but not significantly the gallbladder contraction, and had no effect on plasma CCK secretion. Atropine 0-8 cholecystokinin Homo sapiens 360-363 3509961-5 1987 Atropine (10(-6) M) increased CCK output about 100%. Atropine 0-8 cholecystokinin Homo sapiens 30-33 165733-5 1975 The maximum response of LES muscle to CCK was antagonized only by atropine and tetrodotoxin, but not by other antagonists, suggesting that CCK contracts LES muscle by acetylcholine release. Atropine 66-74 cholecystokinin Homo sapiens 38-41 4035567-5 1985 We repeated the studies giving 300 micrograms/kg of atropine 20 minutes before administration of CCK-8. Atropine 52-60 cholecystokinin Homo sapiens 97-100 3881013-6 1985 Atropine significantly blunted the gallbladder response both to CCK and to CRL. Atropine 0-8 cholecystokinin Homo sapiens 64-67 6096959-0 1984 Atropine inhibits meal-stimulated release of cholecystokinin. Atropine 0-8 cholecystokinin Homo sapiens 45-60 6096959-5 1984 The abolition of measurable CCK release by atropine may entirely account for its inhibitory effects on biliary secretion and in part for its effect on the pancreas. Atropine 43-51 cholecystokinin Homo sapiens 28-31 3535012-5 1986 Enhancement of PP and CCK secretion was almost completely abolished by pretreatment with 1 mg atropine. Atropine 94-102 cholecystokinin Homo sapiens 22-25 6468768-0 1984 Inhibitory effect of atropine on cholecystokinin-induced gallbladder contraction in man. Atropine 21-29 cholecystokinin Homo sapiens 33-48 6468768-1 1984 We have studied the effect of atropine on cholecystokinin (CCK)-induced gallbladder contraction in 7 healthy volunteers by means of real-time ultrasonography. Atropine 30-38 cholecystokinin Homo sapiens 42-57 6468768-1 1984 We have studied the effect of atropine on cholecystokinin (CCK)-induced gallbladder contraction in 7 healthy volunteers by means of real-time ultrasonography. Atropine 30-38 cholecystokinin Homo sapiens 59-62 6468768-8 1984 In 2 subjects in whom a higher dose of atropine, 15 micrograms X kg-1 X h-1, was tested, gallbladder contraction was totally abolished, even when the largest dose of CCK was infused. Atropine 39-47 cholecystokinin Homo sapiens 166-169 6724165-0 1984 Effect of atropine on the plasma cholecystokinin response to intraduodenal fat in man. Atropine 10-18 cholecystokinin Homo sapiens 33-48 6724165-1 1984 The present study was undertaken to determine whether atropine inhibits the plasma cholecystokinin (CCK) response to intraduodenal fat. Atropine 54-62 cholecystokinin Homo sapiens 83-98 6724165-1 1984 The present study was undertaken to determine whether atropine inhibits the plasma cholecystokinin (CCK) response to intraduodenal fat. Atropine 54-62 cholecystokinin Homo sapiens 100-103 6724165-5 1984 Intravenous administration of atropine (0.015 mg/kg as bolus followed by 0.005 mg/kg X h over 3 h) resulted in significant inhibition of plasma CCK concentrations at 10, 20 and 30 min (antibody 1703) and at 20 and 30 min (antibody T204 ) after instillation of fat. Atropine 30-38 cholecystokinin Homo sapiens 144-147 6724165-6 1984 However, the peak increments in plasma CCK during atropine (8.6 +/- 1.9 pmol/l, antibody 1703; 5.4 +/- 1.1 pmol/l, antibody T204 ) were not different from those found without atropine (6.3 +/- 0.8 pmol/l, antibody 1703; 3.9 +/- 0.9 pmol/l, antibody T204 ). Atropine 50-58 cholecystokinin Homo sapiens 39-42 6193036-9 1983 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. Atropine 200-208 cholecystokinin Homo sapiens 46-49 6193036-9 1983 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. Atropine 200-208 cholecystokinin Homo sapiens 46-49 165733-5 1975 The maximum response of LES muscle to CCK was antagonized only by atropine and tetrodotoxin, but not by other antagonists, suggesting that CCK contracts LES muscle by acetylcholine release. Atropine 66-74 cholecystokinin Homo sapiens 139-142 29902066-13 2018 Atropine significantly attenuated the CCK-induced esophageal LMC, prevented crural diaphragm inhibition, and abolished the phase 2 complete LES relaxation. Atropine 0-8 cholecystokinin Homo sapiens 38-41 28242761-9 2017 Maximal atropine pretreatment that completely blocked all the Cch-evoked responses did not affect any of the CCK-8-evoked responses, indicating that rather than acting on the nerves within the pancreas slice, CCK cellular actions directly affected human acinar cells. Atropine 8-16 cholecystokinin Homo sapiens 209-212