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

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 m M-D-glucose was not affected. Potentiation required the presence of Ca²⁺. 2. In bicarbonate buffer, ACh stimulated the islet uptake of ⁴⁵Ca²⁺ at 3 m M-glucose but not significantly at 11 m M; no effect was seen in Tris buffer. 3. At 11 m M-glucose, ACh increased the fluorescence from Ca²⁺-chlorotetracycline in dispersed islet cells; the effect was inhibited by atropine. 4. At both 3 and 11 m M-glucose, ACh stimulated the islet uptake of ²²Na⁺ in 60 min. At 11 m M-glucose, ²²Na⁺ uptake in 5 min was also enhanced significantly, and this effect was inhibited by atropine. 5. At 3 m M-glucose, ACh probably stimulated the islet uptake of ⁸⁶Rb⁺ in 10 min. 6. ACh had no effect on ³⁶Cl⁻ retention at 3 or 11 m M-glucose, or on the oxidation of D-[U-¹⁴C]glucose (11 m M). 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.