Bromocriptine and insulin secretion.

The dopaminergic drug bromocriptine inhibited the release of insulin from isolated mouse pancreatic islets. The effect was counteracted by haloperidol or pimozide. It is suggested that insulin release may be inhibited through activation of D-2 dopaminergic receptors in the pancreatic beta-cells.

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

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 Ca(2+).

Effects of ouabain on insulin release, adenosine 3',5'-monophosphate and guanine 3',5'-monophosphate in pancreatic islets.

Isolated pancreatic islets of noninbred ob/ob mice were used to test the hypothesis that adenylate cyclase responds to changes of the transmembrane milieu or electric field in intact beta-cells. In the presence of a phosphodiesterase inhibitor, ouabainstimulated both the release of insulin and the islet content of cAMP. Ouabain had no noticeable effect on the islet content of cGMP.

Are pancreatic beta-cells under vagal control?

To elucidate the importance of cholinergic innervation for pancreatic beta-cells in vivo, atropine sulphate (0.2 mg/kg body weight) was subcutaneously injected into mice 4 times a day for 10 days. Control animals received 0.