The inhibitory effect of CR-1409 on amylase secretion and intracellular Ca2+ mobilization in rat pancreatic acini in vitro.

A bioassay using dispersed pancreatic acini was used to measure fasting plasma cholecystokinin (CCK) concentrations in 105 patients with various kinds of gastrointestinal diseases, 17 patients with diabetes mellitus, and 6 healthy volunteers. High plasma CCK bioactivities were observed in patients with obstructive jaundice, choledocolithiasis, and primary biliary cirrhosis. Twenty-three samples with high CCK bioactivities were assayed by the same bioassay after the addition of a specific CCK antagonist and by a CCK radioimmunoassay in order to determine whether the high CCK-like bioactivity was due to circulating CCK or other factors. High CCK bioactivities were partially inhibited by the specific CCK antagonist, CR-1409, but the activities were not totally abolished. The residual bioactivities (not inhibited by CR-1409) correlated with plasma bile acid concentrations. The inhibitable CCK bioactivities correlated with plasma CCK levels obtained by radioimmunoassay. Although the bioassay using dispersed pancreatic acini has several advantages for measuring plasma CCK, this method overestimates CCK bioactivities in patients with high plasma bile acid concentrations.

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Bile acids in human plasma interfere with cholecystokinin bioassay using dispersed pancreatic acini

Miyasaka

Funakoshi

Matsumoto

et al. 1991

Digest Dis Sci

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Bioactivity of synthetic human cholecystokinin (CCK)-33 in vitro and in vivo

Shinozaki¹,

Miyasaka

Wakasugi

et al. 1991

Gastroenterol Jpn

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The relative potencies of synthetic human cholecystokinin (h-CCK)-33, porcine CCK-33 (p-CCK-33) and CCK-8 were examined by measuring pancreatic secretion in the conscious rat (in vivo) and amylase release from rat pancreatic acini using a perifusion study (in vitro). The increments of protein output during an 1-hr infusion of 100 pmol/kg/hr of h-CCK-33, p-CCK-33 and CCK-8 were 27.0 +/- 2.9 mg/hr (M +/- SE), 19.3 +/- 2.8 and 14.0 +/- 1.8 mg/hr, respectively. H-CCK-33 and p-CCK-33 showed significantly higher responses of protein output than CCK-8 in a same molar ratio, in vivo. In vitro, the stimulation with 10(-10) M h-CCK-33, p-CCK-33 and CCK-8 led to a similar biphasic amylase release in a perifusion study. Twenty-five microM CR-1409, an antagonist for CCK receptor, completely inhibited the 10(-10) M h-CCK-33-stimulated amylase release. Although it was found that h-CCK-33 and p-CCK-33 were more potent than CCK-8 in vivo, 10(-10) M CCK-8, h-CCK-33 and p-CCK-33 were equipotent on rat pancreatic acini in vitro. It is suggested that the discrepancy in potencies of the large molecular form and small molecular form of CCK in vivo and in vitro may be attributed to the delay of degradation of the large molecular form of CCK in vivo.

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The inhibitory effect of CR-1409 on amylase secretion and intracellular Ca2+ mobilization in rat pancreatic acini in vitro.

Cited by 2 publications

References 19 publications

Bile acids in human plasma interfere with cholecystokinin bioassay using dispersed pancreatic acini

Bile acids in human plasma interfere with cholecystokinin bioassay using dispersed pancreatic acini

Bioactivity of synthetic human cholecystokinin (CCK)-33 in vitro and in vivo

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