B cell adrenoceptors and sulphonylurea-induced insulin release in mouse islets

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Abstract
Interactions of tolbutamide and glibenclamide with B cell adrenoceptors have been reported. This study evaluated the possible role of such interactions in the stimulation of insulin release. Mouse islets were incubated in the presence of 10 mmol/l glucose alone or with tolbutamide (10 μmol/l) or glibenclamide (0.02 μmol/l). At 0.01–10 μmol/l, blockers of α2-adrenoceptors (yohimbine, idazoxan) or α1-adrenoceptors (prazosin) had practically no effect on glucose-induced insulin release and did not affect its potentiation by sulphonylureas, except for a slight increase by 10 μmol/l prazosin and idazoxan. Nonspecific α-blockers (phentolamine, dihydroergotamine) increased control release at 10 μmol/l, but only the latter amplified the response to tolbutamide. Blockers of β-adrenoceptors were tested at 0.1–100 μmol/l: propranolol (β1, β2), metoprolol (β1) and compound ICI 118-551 (β2). They increased glucose-induced insulin release at 100 μmol/l but variably altered the effect of sulphonylureas. Blockers of adrenoceptors have, thus, no effect on insulin release in vitro at therapeutic concentrations. At high concentrations, they non-specifically affect the action of sulphonylureas. We conclude that an interaction with B cell adrenoceptors is not involved in the insulinotropic action of sulphonylureas.