Inhibitory effects of pirenzepine on cholinergic stimulation of exocrine rat pancreas in vitro.

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The effects of pirenzepine on carbamylcholine-stimulated exocrine pancreatic functions were studied in both the isolated pancreatic acini and the isolated perfused pancreas of rats and compared with those of atropine. Pirenzepine and atropine produced a concentration-dependent inhibition of amylase secretion initiated by carbamylcholine. Pirenzepine was, however, about 300 times less potent than atropine on a molar basis in inhibiting the stimulated amylase release. A similar difference in potency was observed with respect to carbamylcholine stimulation of pancreatic juice and amylase release from the isolated perfused pancrease. The inhibitory effect of pirenzepine was fully reversible. Termination of pirenzepine infusion resulted in an immediate increase of both pancreatic juice flow and amylase output to a level comparable to that with carbamylcholine stimulation alone in the corresponding period. In contrast, the recovery of pancreatic exocrine responses after the removal of atropine was slow. The present observations suggest that cholinergic stimulated amylase release from pancreatic acini is mediated by M2 receptors. Since pirenzepine preferentially antagonizes the action of acetylcholine M1 receptor, it seems unlikely that inhibitory doses of pirenzepine on M1 receptor (gastric acid secretion) cause inhibitory effects on M2 receptors.
財団法人日本消化器病学会の論文