PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20852067-7 2010 ACh secretion by PSCs exposed to 20 pM CCK was measured by LC-MS/MS. Acetylcholine 0-3 cholecystokinin Homo sapiens 39-42 20852067-11 2010 CCK stimulates ACh secretion by PSCs, which, in turn, induces amylase secretion by acini. Acetylcholine 15-18 cholecystokinin Homo sapiens 0-3 21525756-2 2010 Cholecystokinin (CCK) stimulates both directly via CCK-A receptors on acinar cells and indirectly via CCK-B receptors on nerves, followed by acetylcholine release, pancreatic enzyme secretion. Acetylcholine 141-154 cholecystokinin Homo sapiens 0-15 21525756-2 2010 Cholecystokinin (CCK) stimulates both directly via CCK-A receptors on acinar cells and indirectly via CCK-B receptors on nerves, followed by acetylcholine release, pancreatic enzyme secretion. Acetylcholine 141-154 cholecystokinin Homo sapiens 17-20 12065595-5 2002 Imaging of fura-2-loaded acinar cells revealed that the rate of [Ca(2+)](c) rise during CCK-evoked oscillations slows with each subsequent oscillation, consistent with a developing modulation of release, whereas the kinetics of ACh-evoked oscillations remain constant. Acetylcholine 228-231 cholecystokinin Homo sapiens 88-91 17027490-5 2006 CCK and ACh recruit Ca(2+) from lysosomes and from zymogen granules through different mechanisms; CCK uses NAADP and cADPR, respectively, and ACh uses Ca(2+) and IP(3), respectively. Acetylcholine 142-145 cholecystokinin Homo sapiens 0-3 12065595-6 2002 Stimulation of cells with ACh following activation of PKA resulted in a slowing of the ACh-evoked [Ca(2+)](c) rise, which now resembled a time-matched CCK response. Acetylcholine 26-29 cholecystokinin Homo sapiens 151-154 12065595-6 2002 Stimulation of cells with ACh following activation of PKA resulted in a slowing of the ACh-evoked [Ca(2+)](c) rise, which now resembled a time-matched CCK response. Acetylcholine 87-90 cholecystokinin Homo sapiens 151-154 12065595-8 2002 Targeted, PKA-mediated phosphorylation of type III InsP(3)R is involved in a physiological CCK response, as disruption of the targeting of PKA with the peptide HT31 resulted in marked changes in the CCK-evoked [Ca(2+)](c) signal but had no effect on ACh-evoked responses. Acetylcholine 250-253 cholecystokinin Homo sapiens 199-202 7773354-7 1995 These observations suggest that: (1) fasting gallbladder tone is influenced by cholinergic inhibitory mechanisms, (2) acetylcholine (ACh) is the final mediator for about 40% of the postprandial gallbladder emptying and pancreatic polypeptide response, and (3) coordination between the ACh-independent cholecystokinin response and ACh-dependent pancreatic polypeptide response may be important in the regulation of postprandial gallbladder emptying. Acetylcholine 133-136 cholecystokinin Homo sapiens 301-316 10672334-5 1998 Similarly to the classic neurotransmitters, CCK and its analogues could play a neurotransmitter role, also modulating the release of acetylcholine (ACh) and of other neurotransmitters in enteric and CNS neurons. Acetylcholine 133-146 cholecystokinin Homo sapiens 44-47 10672334-5 1998 Similarly to the classic neurotransmitters, CCK and its analogues could play a neurotransmitter role, also modulating the release of acetylcholine (ACh) and of other neurotransmitters in enteric and CNS neurons. Acetylcholine 148-151 cholecystokinin Homo sapiens 44-47 8638720-6 1996 S-CCK-8 (10(-8)M) also increased the quantal content and quantal size of nerve-evoked fEPSPs and increased the response to exogenously applied acetylcholine (ACh). Acetylcholine 143-156 cholecystokinin Homo sapiens 2-5 8638720-6 1996 S-CCK-8 (10(-8)M) also increased the quantal content and quantal size of nerve-evoked fEPSPs and increased the response to exogenously applied acetylcholine (ACh). Acetylcholine 158-161 cholecystokinin Homo sapiens 2-5 8638720-8 1996 It was concluded that S-CCK-8 potentiated nicotinic transmission by facilitating release of ACh from preganglionic nerve terminals and by increasing the postsynaptic membrane sensitivity to ACh. Acetylcholine 92-95 cholecystokinin Homo sapiens 24-27 8638720-8 1996 It was concluded that S-CCK-8 potentiated nicotinic transmission by facilitating release of ACh from preganglionic nerve terminals and by increasing the postsynaptic membrane sensitivity to ACh. Acetylcholine 190-193 cholecystokinin Homo sapiens 24-27 7773354-7 1995 These observations suggest that: (1) fasting gallbladder tone is influenced by cholinergic inhibitory mechanisms, (2) acetylcholine (ACh) is the final mediator for about 40% of the postprandial gallbladder emptying and pancreatic polypeptide response, and (3) coordination between the ACh-independent cholecystokinin response and ACh-dependent pancreatic polypeptide response may be important in the regulation of postprandial gallbladder emptying. Acetylcholine 118-131 cholecystokinin Homo sapiens 301-316 1636705-10 1992 Correlative in vitro experiments suggest that CCK may act by stimulation of neural acetylcholine release. Acetylcholine 83-96 cholecystokinin Homo sapiens 46-49 8185161-4 1994 Furthermore, CCK can enhance ongoing nicotinic ganglionic transmission occurring in the serosal layer by release of acetylcholine. Acetylcholine 116-129 cholecystokinin Homo sapiens 13-16 8360161-8 1993 Although initiated by ACh, these transients displayed the temporal and functional characteristics of the CCK-evoked transients. Acetylcholine 22-25 cholecystokinin Homo sapiens 105-108 6651414-5 1983 Concentrations of CCK-4, CCK-6 and CCK-7 producing 50% relaxation of normal tone in circular muscles were 19 microM, and 53 nM, respectively; concentrations producing 50% inhibition of ACh-induced contraction in longitudinal muscle were 20, 13 and 47 microM, respectively. Acetylcholine 185-188 cholecystokinin Homo sapiens 18-21 2192849-14 1990 An important new insight is provided by the observation that agonists (e.g., CCK or acetylcholine) that act to stimulate the hydrolysis of phosphatidylinositides, when acting for a short period (10-20 min), induce an enhanced responsiveness of islets to glucose, i.e., proemial sensitization. Acetylcholine 84-97 cholecystokinin Homo sapiens 77-80 6651414-5 1983 Concentrations of CCK-4, CCK-6 and CCK-7 producing 50% relaxation of normal tone in circular muscles were 19 microM, and 53 nM, respectively; concentrations producing 50% inhibition of ACh-induced contraction in longitudinal muscle were 20, 13 and 47 microM, respectively. Acetylcholine 185-188 cholecystokinin Homo sapiens 25-28 24190932-10 2014 The low-frequency IPSC oscillations induced by CCh or optogenetically stimulated ACh release were also inhibited by a mu-opioid receptor (MOR) agonist, which was unexpected because MORs in CA1 are not usually associated with CCK-expressing cells. Acetylcholine 81-84 cholecystokinin Homo sapiens 225-228 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. Acetylcholine 167-180 cholecystokinin Homo sapiens 38-41 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. Acetylcholine 167-180 cholecystokinin Homo sapiens 139-142 31108325-18 2019 The correlation analysis revealed negative correlations between Ach levels and inflammation (p < .001), and a positive correlation between CCK and Ach levels (r = 0.775, p < .001). Acetylcholine 147-150 cholecystokinin Homo sapiens 139-142 31108325-22 2019 Additionally, the multivariate linear regression analysis identified EEN, plasma lactate, mechanical ventilation, the SOFA score and plasma CCK levels as independent determinants of plasma Ach levels. Acetylcholine 189-192 cholecystokinin Homo sapiens 140-143 31108325-24 2019 The effect of EEN on Ach levels is partially attributed to the increase in CCK levels. Acetylcholine 21-24 cholecystokinin Homo sapiens 75-78