AJP - Gastrointestinal and Liver Physiology, Vol 250, Issue 5 665-G669, Copyright © 1986 by American Physiological Society
Contrasting cholinergic dependence of pancreatic and gallbladder responses to cholecystokinin
K. M. Strah, T. N. Pappas, R. L. Melendez and H. T. Debas
Cholinergic receptors for cholecystokinin (CCK) have been identified on
neurons of the enteric nervous system, including those of the gallbladder.
To determine whether any differences exist in the extent to which CCK
action depends on muscarinic cholinergic receptors in the pancreas and
gallbladder, 11 dogs with pancreatic and 7 dogs with biliary fistulas were
given increasing doses of intravenous CCK-8 (15-250 ng X kg-1 X h-1) or
intraduodenal sodium oleate (0.1-9 mmol/h) with and without atropine
pretreatment. Pancreatic protein response to CCK-8 was dose dependent,
reaching a maximal of 448 +/- 76 mg/15 min at the highest dose. Atropine
pretreatment caused nonsignificant reduction in the response to the lowest
dose but had no effect on the responses to the other doses, with the
response to the highest dose of CCK being 473 +/- 82 mg/15 min. In
contrast, gallbladder contraction as measured by bile fistula bilirubin
output was very sensitive to inhibition by atropine. Bilirubin responses to
16, 32, 62.5, 125, and 250 ng X kg-1 X h-1 were 14 +/- 5, 18 +/- 5, 28 +/-
5, 36 +/- 6, and 52 +/- 12 mg/h, respectively, without atropine and 0 +/-
0, 6 +/- 2, 7 +/- 2, 18 +/- 4, and 18 +/- 4 mg/h with atropine
pretreatment. Similarly, pancreatic responses to sodium oleate infusion
were less susceptible to inhibition by atropine than were the gallbladder
responses. With respect to pancreatic protein secretion, the response to
only the lowest dose of sodium oleate was significantly inhibited by
atropine.(ABSTRACT TRUNCATED AT 250 WORDS)
