Pancreatic secretion stimulated by endogenous cholecystokinin is not mediated by capsaicin-sensitive vagal afferent pathway in awake rats. Guan, Difu, William T. Phillips, and Gary M. Green. Departments of Physiology and Radiology, University of Texas Health Science Center, San Antonio, TX 78284
APStracts 3:0043G, 1996.
A capsaicin-sensitive vagal afferent pathway was reported to mediate the effect of endogenous CCK on pancreatic secretion in anesthetized rats. Because neural blockade affects pancreatic secretion much less in awake than in anesthetized rats, the effect of capsaicin-ablation of vagal afferent pathways on pancreatic secretion stimulated by endogenous CCK was examined in awake rats. During surgery, abdominal vagal trunks were exposed and 0.1 ml of capsaicin (10 mg/ml), was applied to the vagal trunks. Ablation of vagal afferent pathway was assessed by the ability of intraperitoneal CCK-8 to suppress food intake and inhibit gastric emptying. Endogenous CCK release was stimulated by diversion of bile-pancreatic juice from the intestine and by intraduodenal infusion of casein. Pancreatic protein and fluid secretion were significantly increased by both treatments and the responses were unaffected by capsaicin. CCK-8, i.p., markedly inhibited food intake and gastric emptying and both effects were significantly attenuated in capsaicin-treated rats, indicating that capsaicin treatment successfully ablated afferent vagal fibers. It is concluded that CCK-stimulated pancreatic secretion in rats is not mediated by a vagal afferent pathway. 

Received 4 December 1995; accepted in final form 5 February 1996.
APS Manuscript Number G510-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 24 February 96