HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Chandler, D. E. Articles by Williams, J. A. Search for Related Content PubMed PubMed Citation Articles by Chandler, D. E. Articles by Williams, J. A.

1. The effect of La³⁺ on amylase release and Ca²⁺ fluxes in mouse pancreatic fragments in vitro was studied.

2. Amylase release was increased by 0·1 mM-La³⁺ and progressively inhibited by 1·0-10 mM-La³⁺. Non-stimulated and bethanecol stimulated secretion were altered in an identical manner. Inhibition of amylase release was rapid and reversible.

3. Uptake of ⁴⁵Ca²⁺ was multiphasic with equilibrium with stable Ca²⁺ still not complete after 2 hr. La³⁺ (10 mM) limited uptake of ⁴⁵Ca²⁺ to the extracellular space and slightly decreased total Ca²⁺ content. Lower concentrations of La³⁺ affected ⁴⁵Ca²⁺ uptake and total Ca²⁺ content in a biphasic manner which paralleled effects on amylase release.

4. La³⁺ restricted washout of ⁴⁵Ca²⁺ to isotope in the extracellular space and abolished the bethanecol-stimulated increase in ⁴⁵Ca²⁺ efflux.

5. Uptake of ⁴⁵Ca²⁺ into intracellular space, as measured by the `lanthanum' method, was not affected by bethanecol.

6. Tissue ultrastructure and Na⁺ and K⁺ content were not affected by La³⁺.

7. It is concluded that an influx of extracellular Ca²⁺ is not important for triggering of secretion and that La³⁺ may inhibit amylase release by acting on the release process rather than on Ca²⁺ influx.