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Effect of nicotine on exocytotic pancreatic secretory response: role of calcium signaling

Parimal Chowdhury1* and Kodetthoor B Udupa123

Author Affiliations

1 Department of Physiology & Biophysics, University of Arkansas for Medical Sciences, College of Medicine, 4301 W Markham Street, Little Rock, 72205, Arkansas

2 Formerly at Donald W. Reynolds Department of Geriatrics, University of Arkansas for Medical sciences, College of Medicine, 4301 W Markham Street, Little Rock, 72205, Arkansas

3 Formerly in Medical Research, Central Arkansas Veterans Health Care System, Little Rock, Arkansas

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Tobacco Induced Diseases 2013, 11:1  doi:10.1186/1617-9625-11-1

Published: 18 January 2013



Nicotine is a risk factor for pancreatitis resulting in loss of pancreatic enzyme secretion. The aim of this study was to evaluate the mechanisms of nicotine-induced secretory response measured in primary pancreatic acinar cells isolated from Male Sprague Dawley rats. The study examines the role of calcium signaling in the mechanism of the enhanced secretory response observed with nicotine exposure.


Isolated and purified pancreatic acinar cells were subjected to a nicotine exposure at a dose of 100 μM for 6 minutes and then stimulated with cholecystokinin (CCK) for 30 min. The cell’s secretory response was measured by the percent of amylase released from the cells in the incubation medium Calcium receptor antagonists, inositol trisphosphate (IP3) receptor blockers, mitogen activated protein kinase inhibitors and specific nicotinic receptor antagonists were used to confirm the involvement of calcium in this process.


Nicotine exposure induced enhanced secretory response in primary cells. These responses remained unaffected by mitogen activated protein kinases (MAPK’s) inhibitors. The effects, however, have been completely abolished by nicotinic receptor antagonist, calcium channel receptor antagonists and inositol trisphosphate (IP3) receptor blockers.


The data suggest that calcium activated events regulating the exocytotic secretion are affected by nicotine as shown by enhanced functional response which is inhibited by specific antagonists… The results implicate the role of nicotine in the mobilization of both intra- and extracellular calcium in the regulation of stimulus-secretory response of enzyme secretion in this cell system. We conclude that nicotine plays an important role in promoting enhanced calcium levels inside the acinar cell.

Isolated pancreatic acinar cell; Nicotine; Receptor blocker; Calcium channel antagonists; MAPK kinase inhibitors