Mechanism of scorpion toxin-induced enzyme secretion in rat pancreas

Abstract

Scorpion venom induces acute pancreatitis in humans and stimulates pancreatic hypersecretion in several animal species. To clarify whether scorpion toxin influences pancreatic function directly by stimulating the acinar cells or influences pancreatic function indirectly by stimulating pancreatic nerves, we measured amylase release from both rat pancreas lobules (containing both acinar cells and nerves) and isolated rat pancreatic acini (acinar cells only). Scorpion toxin stimulated amylase release from lobules to a similar extent as did carbamylcholine, an acetylcholine agonist. In these lobules, the effect of scorpion toxin was blocked by both atropine (an inhibitor of the cholinergic receptor on acinar cells) and tetrodotoxin (a selective blocker of Na+ channels in nerves). In contrast, the effect of carbamylcholine was blocked by atropine, but not by tetrodotoxin. In isolated pancreatic acini, carbamylcholine was without effect. We conclude that scorpion toxin influences pancreatic function indirectly by stimulating the release of acetylcholine from pancreatic nerves.