Effect of tetracaine and lidocaine on insulin release in isolated mouse pancreatic islets

Abstract

The effect of tetracaine and lidocaine on insulin secretion and glucose oxidation by islets of ob/ob-mice was measured. Tetracaine, at a concentration of 1 μM to 0.1 mM, did not markedly influence the basal (3 mM glucose) insulin secretion, whereas 0.5–3.5 mM induced a marked increase. At 7 mM glucose, there was a dose-dependent increase with 0.1–2.5 mM tetracaine. Insulin release induced by 20 mM glucose was potentiated by 0.1 mM and 0.5 mM tetracaine, but this effect disappeared at 1 mM tetracaine. The stimulatory effect of 0.5–1 mM tetracaine on basal insulin release was blocked by the secretory inhibitors, adrenalin (1 μM), clonidine (1 μM) and by Ca 2+-deficiency, but the stimulation by 3.5 mM tetracaine was not reduced by 1 μM clonidine or Ca 2+ deficiency. Atropin (10 μM) did not affect the stimulation by 0.5 mM tetracaine at 3 mM glucose or by 0.25 mM tetracaine at 20 mM glucose. Tetracaine, at 0.1 mM, potentiated the secretory stimulation of 20 mM l-leucine, 20 mM d-mannose, or 1 μM glibenclamide. Mannoheptulose, 10 mM, abolished the combined effects of 0.1 mM tetracaine and 10 mM glucose. Lidocaine, 1–5 mM, stimulated basal insulin release, but 1 μM–1 mM of the drug did not affect glucose-induced (20 mM glucose) insulin release and 5 mM lidocaine inhibited glucose stimulation. The oxidation of 10 mM d-[U- 14C]glucose was slightly enhanced by 0.1 and 1 mM tetracaine. The results indicate that tetracaine and lidocaine, at certain concentrations, can induce insulin release and that tetracaine potentiates secretion induced by other secretagogues. It is concluded that these effects may be associated with β-cell functions related to the adrenergic receptors but probably not to cholinergic receptors.