AJP - Gastrointestinal and Liver Physiology, Vol 263, Issue 1 12-G16, Copyright © 1992 by American Physiological Society
Neurohormonal mechanism of pancreatic exocrine secretion stimulated by sodium oleate and L-tryptophan in dogs
Y. H. Jo, Y. L. Lee, K. Y. Lee, T. M. Chang and W. Y. Chey
Genesee Hospital, University of Rochester School of Medicine and Dentistry, New York 14607.
In the present investigation, we have studied the effect of atropine on the
pancreatic secretion stimulated by intraduodenal administration of either
sodium oleate or exogenous cholecystokinin (CCK). In four dogs prepared
with gastric and Thomas duodenal cannulas, pancreatic juice was collected
for measurement of volume, bicarbonate, and protein output, and peripheral
venous blood samples were obtained for radioimmunoassay of both secretin
and CCK. Volume, bicarbonate, and protein output of the pancreatic juice
increased significantly in response to sodium oleate (1-4 mmol/h) in a
dose-dependent manner. The increase in pancreatic secretion paralleled the
increments in both plasma CCK and secretin. Atropine given intravenously
suppressed completely both pancreatic secretion and release of CCK
stimulated by sodium oleate, whereas the release of secretin was not
affected. Pancreatic secretion was significantly increased in a
dose-dependent manner by exogenous CCK octapeptide (CCK-8) at 16, 32, and
64 micrograms (14, 28, and 56 pmol).kg-1.h-1. Atropine inhibited protein
output only partially, but it did not influence bicarbonate output. In five
additional dogs, the effect of atropine on L-tryptophan-stimulated
pancreatic secretion was studied. Interestingly, atropine failed to
influence the CCK release and pancreatic secretion of volume and
bicarbonate, except for protein secretion, which was significantly
inhibited. It was shown previously that atropine inhibited significantly
the pancreatic secretion of bicarbonate stimulated by secretin in
physiological doses. Thus we conclude that the inhibition by atropine of
the pancreatic exocrine secretion stimulated by sodium oleate is mediated
by both suppression of CCK release and inhibition of action of secretin on
the exocrine pancreas.(ABSTRACT TRUNCATED AT 250 WORDS)
