Effects of intraduodenal administration of tarazepide on pancreatic secretion and duodenal EMG in neonatal calves

  • Regul Pept. 1998 Nov 30;78(1-3):113-23. doi: 10.1016/s0167-0115(98)00139-6.
R Zabielski  1 ,  V Leśniewska ,  J Borlak ,  P C Gregory ,  P Kiela ,  S G Pierzynowski ,  W Barej
Affiliations
  • 1. Department of Animal Physiology, Warsaw Agricultural University, Poland. [email protected]
PMID: 9879754 DOI: 10.1016/s0167-0115(98)00139-6
Abstract

The influence of CCK-A receptor antagonism on pancreatic exocrine secretion and duodenal EMG, and the mechanism(s) involved in CCK-induced pancreatic secretion were studied in conscious calves. Seven 1-week-old calves were fitted with a pancreatic duct catheter, duodenal cannula and duodenal electrodes. Pancreatic exocrine secretion and duodenal EMG were studied following intraduodenal CCK-A receptor antagonist (Tarazepide), intravenous atropine, and intravenous or intraduodenal CCK-8 administrations. Tarazepide decreased duodenal electric activity, reduced interdigestive pancreatic secretion, especially protein; reduced cephalic and early postprandial (milk) induced secretion of bicarbonate and protein. Pancreatic protein secretion to intravenous CCK-8 was little affected by atropine, but was significantly reduced by Tarazepide+/-atropine; in contrast, protein secretion to intraduodenal CCK-8 was abolished by Tarazepide or atropine. We conclude that pre- and especially early postprandial pancreatic secretion are partly controlled via CCK-A (mainly mucosal) mediated mechanisms.

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