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Role of PACAP 1 Receptor in Regulation of ECL Cells and Gastric Acid Secretion by Pituitary Adenylate Cyclase Activating Peptide
Author(s) -
PISEGNA JOSEPH R.,
OHNING GORDON V.,
ATHMANN CHRISTOPHE,
ZENG NINGXIN,
WALSH JOHN H.,
SACHS GEORGE
Publication year - 2000
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2000.tb06971.x
Subject(s) - enterochromaffin like cell , secretion , histamine , endocrinology , gastric acid , medicine , stimulation , adenylate kinase , chemistry , receptor , pituitary adenylate cyclase activating peptide , parietal cell , biology , neuropeptide , vasoactive intestinal peptide
A bstract : We previously reported that PAC 1 is expressed on ECL cells resulting in stimulation of [Ca 2+ ] i , histamine and acid secretion. The study reported here characterized the signaling by PAC 1m on ECL cells; determined the effects of PACAP on the gastric acid secretion in vivo , and determined the effects of chronic administration of PACAP‐27 on ECL cell proliferation. PACAP‐27 dose dependently stimulated ECL cell Ca 2+ and AC with detectable stimulation at 1 nM and maximal stimulation at 100 nM (six‐fold). In rats PACAP‐27 administration (10 pmol/kg/h) increased the rate of gastric acid secretion when an antisomatostatin antibody was co‐administered. Chronic administration of PACAP (10 pmol/h for seven days) via osmotic pump resulted in a more than twofold increase in BrdU incorporation into ECL cells. PACAP acting at the PAC 1 results in dual signaling responses to both [Ca 2+ ] i . AC in ECL cells stimulates gastric acid secretion via the actions of histamine acting at the parietal cell and in whole animals leads to proliferation of ECL cells when administered chronically.