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Am J Physiol Regul Integr Comp Physiol 281: R645-R653, 2001;
0363-6119/01 $5.00
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Vol. 281, Issue 2, R645-R653, August 2001

PYY inhibits CCK-stimulated pancreatic secretion through the area postrema in unanesthetized rats

Xiaoying Deng1, Dulce R. Guarita1, Martha R. A. Pedroso1, Christianna Kreiss1, Paul G. Wood1, Alan F. Sved2, and David C. Whitcomb1,3,4

1 Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, Departments of 2 Neuroscience and 3 Cell Biology and Physiology, University of Pittsburgh, and 4 Pittsburgh Veterans Affairs Medical Center, Pittsburgh, Pennsylvania 15261

Peptide YY (PYY) inhibits CCK-8-secretin-stimulated pancreatic secretion in vivo. To investigate whether CCK-8-secretin-stimulated pancreatic secretion is mediated through a vago-vagal pathway and whether PYY inhibits this pathway through the area postrema (AP), chronic pancreatic, biliary, and duodenal catheters were implanted in AP-lesioned (APX) or sham-operated rats. The effects of APX on pancreatic secretion stimulated by bethanechol, pancreatic juice diversion (PJD), or CCK-8-secretin, were tested, with and without background PYY infusion, in unanesthetized rats. APX reduced basal pancreatic secretion by 15-20% (P < 0.01). APX had no effect on bethanechol-stimulated secretion and potentiated protein secretion stimulated by PJD (396 vs. 284%) and exogenous CCK-8-secretin. In sham-operated rats, background PYY potently inhibited CCK-8-secretin-stimulated pancreatic fluid (1.8 vs. 48.2%) and protein secretion (3.7 vs. 45.8%) but potentiated fluid (52.9 vs. 43.1%) and protein (132.9 vs. 68.9%) secretion in APX rats. Our findings demonstrate that PYY inhibits CCK-8-secretin-stimulated pancreatic secretion through an AP-dependent mechanism in sham-operated rats. The AP also contributes to basal pancreatic secretion.

peptide YY; cholecystokinin; area postrema lesion; pancreatic exocrine secretion


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