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. 1980;300:505–513. doi: 10.1113/jphysiol.1980.sp013175

Effects of acetylcholine on ion fluxes and chlorotetracycline fluorescence in pancreatic islets

E Gagerman 1, J Sehlin 1, I-B Täljedal 1
PMCID: PMC1279368  PMID: 6991671

Abstract

1. Acetylcholine potentiated glucose-stimulated insulin release from ob/ob-mouse islets in salt-balanced bicarbonate buffer and to a lesser extent in Tris buffer; basal insulin release at 3 mM-D-glucose was not affected. Potentiation required the presence of Ca2+.

2. In bicarbonate buffer, ACh stimulated the islet uptake of 45Ca2+ at 3 mM-glucose but not significantly at 11 mM; no effect was seen in Tris buffer.

3. At 11 mM-glucose, ACh increased the fluorescence from Ca2+-chlorotetracycline in dispersed islet cells; the effect was inhibited by atropine.

4. At both 3 and 11 mM-glucose, ACh stimulated the islet uptake of 22Na+ in 60 min. At 11 mM-glucose, 22Na+ uptake in 5 min was also enhanced significantly, and this effect was inhibited by atropine.

5. At 3 mM-glucose, ACh probably stimulated the islet uptake of 86Rb+ in 10 min.

6. ACh had no effect on 36Cl- retention at 3 or 11 mM-glucose, or on the oxidation of D-[U-14C]glucose (11 mM).

7. The insulin secretory potentiator, ACh, does not act by accelerating glucose oxidation and does not induce the same ionic effects as the secretory initiator, D-glucose. Increased Na+ permeability and altered interaction of Ca2+ with the plasma membrane may play roles in the cholinergic depolarization of β-cells and potentiation of insulin release.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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