Cadmium inhibits stimulated amylase secretion from isolated pancreatic lobules of the guinea-pig.
The effect of cadmium chloride on pancreatic exocrine secretion 'in vitro' was examined using guinea-pig isolated lobules. Cadmium (10(-3)M) stimulated amylase release when added alone to the incubation medium and the increase of amylase was unaffected by atropine. Cadmium (10(-4)M) did not significantly modify the basal amylase release. Depolarization of pancreatic nerves with potassium stimulated amylase secretion; the stimulant effect of KCl was completely inhibited by atropine. Cadmium (10(-4)M) inhibited, but did not abolish, the stimulant effect of KCl, indicating a direct effect of the metal on the acinar cell. Cadmium (10(-4)M) also inhibited the amylase release evoked by the secretagogues carbachol and caerulein, which are known to act directly on the acinar cell. Taken together with previous data reporting a large increase of pancreatic cadmium concentration following cadmium ingestion, the strong inhibition of pancreatic secretion observed in our experiments suggests that the exocrine pancreas may be regarded as a possible target organ of cadmium toxicity.
Linari
G
G
Department of Human Physiology and Pharmacology, Faculty of Medicine, University La Sapienza, Rome, Italy. glinari@uniroma1.it
Nencini
P
P
Nucerito
V
V
D000681:Amylases / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D002104:Cadmium / Q000494:pharmacology*; D002217:Carbachol / Q000494:pharmacology; D002108:Ceruletide / Q000494:pharmacology; D004347:Drug Interactions; D005765:Gastrointestinal Agents / Q000494:pharmacology; D006168:Guinea Pigs; D010179:Pancreas / Q000187:drug effects* / Q000201:enzymology; D011188:Potassium / Q000494:pharmacology
D005765:Gastrointestinal Agents; D002104:Cadmium; D002108:Ceruletide; D002217:Carbachol; D000681:Amylases; D011188:Potassium