AJP - Gastrointestinal and Liver Physiology, Vol 253, Issue 4 445-G451, Copyright © 1987 by American Physiological Society
Receptor-mediated internalization and secretion of cholecystokinin into rat pancreatic duct fluid
R. S. Izzo and M. Praissman
Department of Medicine, Nassau County Medical Center, East Meadow, New York 11554.
We measured cholecystokinin (CCK) in pancreatic duct secretions (PDS) after
infusion of different amounts of CCK-8 (the C-terminal octapeptide of
cholecystokinin) into rats. Injection of 23, 46, and 92 ng of CCK-8
increased immunoreactive cholecystokinin in PDS by 3-, 13-, and 28-fold
above basal levels within 30 min. Continuous intravenous infusion of CCK-8
(50 ng/min) into rats for 30 min, followed by a 30-min rest period, and
then a final infusion of peptide for another 30 min increased CCK in PDS
only during the final period by 12-fold to 500 pg/30 min. Neither gastrin
nor oxidized CCK-8 were detected in PDS after intravenous infusion of each
peptide. Administration of proglumide (ip), a CCK receptor antagonist,
during continuous CCK infusion significantly reduced immunoreactive CCK
levels in PDS to 2% of the control group (P less than or equal to 0.01).
CCK was also rapidly internalized into dispersed pancreatic acinar cells in
a temperature-dependent fashion, and this process was inhibited by
proglumide. The above data suggest that CCK in PDS reflects a
peptide-specific process that is receptor mediated. We propose that
circulating cholecystokinin binds to specific receptors on pancreatic
acinar cells, is internalized, and is then secreted into pancreatic duct
fluid.
