Gastroenterology
Volume 80, Issue 5, Part 1 , Pages 970-973, May 1981

Mechanism of scorpion toxin-induced enzyme secretion in rat pancreas☆

  • Steven Gallagher

      Affiliations

    • Cell Biology Research Laboratory and Department of Medicine, Mount Zion Hospital and Medical Center, San Francisco, California, USA
    • Department of Physiology, University of California, San Francisco, California, USA
    • ,
  • Hariharan Sankaran

      Affiliations

    • Cell Biology Research Laboratory and Department of Medicine, Mount Zion Hospital and Medical Center, San Francisco, California, USA
    • Department of Physiology, University of California, San Francisco, California, USA
    • Dr. Hariharan Sankaran was supported by a NIH postdoctoral fellowship from the NIAMDD.
    • ,
  • John A. Williams

      Affiliations

    • Corresponding Author InformationAddress requests for reprints to: Dr. John A. Williams, Cell Biology Research Laboratory, Mount Zion Hospital and Medical Center, P.O. Box 7921, San Francisco, California 94120.
    • Cell Biology Research Laboratory and Department of Medicine, Mount Zion Hospital and Medical Center, San Francisco, California, USA
    • Department of Physiology, University of California, San Francisco, California, USA

Received 3 November 1980; accepted 11 December 1980.

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 pancreatic 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 stimulated amylase release, but scorpion toxin was without effect. We conclude that scorpion toxin influences pancreatic function indirectly by stimulating the release of acetylcholine from pancreatic nerves.

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☆ This research was supported by NIH grant GM19998 and the Elise Stern Haas Research Fund, Harold Brunn Institute, of Mount Zion Hospital and Medical Center.

PII: 0016-5085(81)90067-6

Gastroenterology
Volume 80, Issue 5, Part 1 , Pages 970-973, May 1981

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