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Insulin secretion from isolated rat islets of Langerhans in the presence of 4 mM glucose averaged 2·26 ± 0·20 (S.E.M.) ng/islet per 90 min and was significantly (P<0·001; n=30) increased to 3·28 ± 0·21 ng/islet per 90 min by the covalent -adrenoceptor antagonist benextramine (10 µM). Glucose (20 mM) also increased the secretion rate (to 6·24 ± 6·0 ng/islet per 90 min) but, under these conditions, the response was not further enhanced by benextramine. Clonidine and noradrenaline (1 nM–10 µM) each caused dose-dependent inhibition of glucose-induced insulin secretion which was maximal at 1 µM. Benextramine, when added simultaneously with the agonist, relieved, in a dosedependent manner, the inhibition of secretion induced by either clonidine or noradrenaline with similar sensitivity. Even after a 30-min preincubation with benextramine the antagonist failed to differentiate between noradrenaline, adrenaline and clonidine with respect to inhibition of insulin secretion. In contrast to its effects on adrenergic responses, short-term treatment with benextramine did not significantly affect muscarinic—cholinergic receptor-mediated ⁴⁵Ca²⁺ efflux from rat islets of Langerhans perifused in Ca²⁺-depleted medium. These data suggest that benextramine does not differentiate between clonidine and noradrenaline in rat islets of Langerhans but that it does show preference for -adrenoceptors in this tissue.