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Am J Physiol Gastrointest Liver Physiol 274: G734-G741, 1998;
0193-1857/98 $5.00
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Vol. 274, Issue 4, G734-G741, April 1998

Telenzepine-sensitive muscarinic receptors on rat pancreatic acinar cells

Stefan W. Schmid1,2, Irvin M. Modlin1, Laura H. Tang1, Aubry Stoch1, Steve Rhee1, Michael H. Nathanson1, George A. Scheele3, and Fred S. Gorelick1

1 Departments of Surgery, Medicine, and Cell Biology, Connecticut Health Care Department of Veterans Affairs, West Haven, and Yale University School of Medicine, New Haven, Connecticut 06516; 2 Department of Visceral and Transplantation Surgery, University of Bern, 3010 Bern, Switzerland; and 3 AlphaGene, Inc., Charlestown, Massachusetts 02129

To identify the muscarinic subtype present on the rat pancreatic acinar cell, we examined the effects of different muscarinic receptor antagonists on amylase secretion and proteolytic zymogen processing in isolated rat pancreatic acini. Maximal zymogen processing required a concentration of carbachol 10- to 100-fold greater (10-3 M) than that required for maximal amylase secretion (10-5 M). Although both secretion and conversion were inhibited by the M3 antagonist 4-diphenylacetoxy-N-methyl-piperidine (4-DAMP) (50% inhibition ~6 × 10-7 M and 1 × 10-8 M, respectively), the most potent inhibitor was the M1 antagonist telenzepine (50% inhibition ~5 × 10-10 M and 1 × 10-11 M, respectively). Pirenzepine, another M1 antagonist, and the M2 antagonist methoctramine did not reduce amylase secretion or zymogen processing in concentrations up to 1 × 10-5 M. Analysis of acinar cell muscarinic receptor by PCR revealed expression of both m1 and m3 subtypes. The pancreatic acinar cell has a distinct pattern of muscarinic antagonist sensitivity (telenzepine >>  4-DAMP > pirenzepine) with respect to both amylase secretion and zymogen conversion.

muscarinic antagonist; 4-diphenylacetoxy-N-methyl-piperidine; carboxypeptidase A1; secretion


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