HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 286/1/R189    most recent 00265.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Xiao, R. Articles by Cui, Z. J. Search for Related Content PubMed PubMed Citation Articles by Xiao, R. Articles by Cui, Z. J.

APPETITE, OBESITY AND METABOLISM

Mutual dependence of VIP/PACAP and CCK receptor signaling for a physiological role in duck exocrine pancreatic secretion

Institute of Cell Biology, Beijing Normal University, Beijing 100875, China

Submitted 12 May 2003 ; accepted in final form 22 August 2003

Unlike in rodents, CCK has not been established as a physiological regulator in avian exocrine pancreatic secretion. In the isolated duck pancreatic acini, 1 nM CCK was required for stimulation of amylase secretion, maximal effect being achieved at 10 nM; picomolar CCK was without effect. Vasoactive intestinal peptide (VIP)/pituitary adenylate cyclase activating peptide (PACAP) receptor (VPAC) agonists PACAP-38 and PACAP-27 (10^-12-10^-7 M) alone had no effect, but made picomolar CCK effective. VPAC agonist VIP 10^-10-10^-7 M stimulated amylase secretion marginally, but made CCK 10^-12-10^-10 M effective also. PACAP-27 and VIP both shifted the maximal CCK concentration from 10^-8 to 10^-9 M. This sensitizing effect was mimicked by forskolin. CCK dose dependently induced intracellular Ca²⁺ concentration ([Ca²⁺]_i) oscillations. PACAP-38 (1 nM), PACAP-27 (1 nM), VIP (10 nM), or forskolin (10 µM) alone did not stimulate [Ca²⁺]_i increase, neither did they modulate CCK (1 nM)-induced oscillations; but when they were added to cells simultaneously exposed to subthreshold CCK (10 pM), calcium spikes emerged. Amylase secretion induced by the simultaneous presence of 10 pM CCK and VPAC agonists was completely blocked by removing extracellular calcium, but the protein kinase C inhibitor staurosporine (1 µM) was without effect. CCK (10 nM)-induced secretion was inhibited by CCK₁ receptor antagonist FK480 (1 µM). Gastrin from 10^-12 to 10^-6 M did not stimulate amylase secretion nor did it (100 nM) induce [Ca²⁺]_i increase. The above data suggest that duck pancreatic acini possess both CCK₁ and VPAC receptors; simultaneous activation of both is required for each to play a physiological role.

amylase secretion; calcium oscillation; pancreatic acinar cell

This article has been cited by other articles:

				Y. Decker, G. McBean, and C. Godson Lipoxin A4 inhibits IL-1{beta}-induced IL-8 and ICAM-1 expression in 1321N1 human astrocytoma cells Am J Physiol Cell Physiol, June 1, 2009; 296(6): C1420 - C1427. [Abstract] [Full Text] [PDF]

				B. J. Wang and Z. J. Cui How does cholecystokinin stimulate exocrine pancreatic secretion? From birds, rodents, to humans Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2007; 292(2): R666 - R678. [Abstract] [Full Text] [PDF]