Abstract

The effect of cadmium chloride on pancreatic exocrine secretion ‘in vitro’ was examined using guinea-pig isolated lobules. Cadmium (10−3M) stimulated amylase release when added alone to the incubation medium and the increase of amylase was unaffected by atropine. Cadmium (10−4M) 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 (10−4M) inhibited, but did not abolish, the stimulant effect of KCl, indicating a direct effect of the metal on the acinar cell. Cadmium (10−4M) 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.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.