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An Investigative study on the mechanisms by which nicotine affects the secretory responses in rat primary pancreatic acinar cells
Author(s) -
Chowdhury Parimal,
Udupa Kodetthoor B.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1349-c
Subject(s) - mecamylamine , endocrinology , nicotine , medicine , chemistry , calcium in biology , cholecystokinin , calcium , receptor , cholecystokinin receptor , extracellular , inositol trisphosphate , intracellular , nicotinic agonist , biology , inositol , biochemistry
The current study examined the underlying mechanisms behind the nicotine –induced maximal secretory response to cholecystokinin ( CCK) in isolated pancreatic acinar cells. Methods: Acinar cells were isolated, purified and maintained in Hepes‐Ringer buffer (HR) at pH 7.4. The cells were incubated with nicotine (100 uM) for 6 min and then with CCK (100pM) for 30 min in the presence or absence of a nicotinic receptor antagonist, calcium receptor antagonists and mitogen activated protein kinase inhibitors. Functional response, measured as an index of percent amylase release in response to CCK, in the incubation media was determined. Results: Exposure of cells to (100 uM)of nicotine significantly enhanced CCK‐stimulated cell function. These effects remained unaltered in the presence of MAPK inhibitors but were suppressed by calcium channel receptor antagonists and inositol trisphosphate (IP3) receptor blockers, p <0.05. Mecamylamine, a nicotinic receptor antagonist, also prevented calcium mobilization resulting in decreased release of amylase in the presence of nicotine. Conclusions: These data suggest that downstream events regulating the exocytotic secretion of amylase in response to CCK in acinar cells are influenced primarily by intracellular calcium release. The results further implicate the role of nicotine in the mobilization of intracellular and extracellular calcium pools in isolated acinar cells. We conclude that nicotine plays an important role in calcium mobilization in acinar cells.