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Effects of acetylcholine on ion fluxes and chlorotetracycline fluorescence in pancreatic islets
Author(s) -
Gagerman E.,
Sehlin J.,
Täljedal I.-B.
Publication year - 1980
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1980.sp013175
Subject(s) - chemistry , medicine , acetylcholine , insulin , endocrinology , islet , bicarbonate , pancreatic islets , depolarization , l glucose , cholinergic , tris , biochemistry , biology
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 Ca 2+ . 2. In bicarbonate buffer, ACh stimulated the islet uptake of 45 Ca 2+ 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 Ca 2+ ‐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 22 Na + in 60 min. At 11 m M ‐glucose, 22 Na + 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 86 Rb + in 10 min. 6. ACh had no effect on 36 Cl − retention at 3 or 11 m M ‐glucose, or on the oxidation of D ‐[U‐ 14 C]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 Ca 2+ with the plasma membrane may play roles in the cholinergic depolarization of β‐cells and potentiation of insulin release.