Immediate and deferred effects of agents stimulating or inhibiting α or β adrenergic receptors have been studied in a perifusion preparation of rat pancreas in which glucose induces a biphasio pattern of IRI release. Epinephrine directly inhibited both the primary and the secondary phases of IRI release during the period of glucose stimulation. Propranolol inhibited only the secondary response. Low concentrations of isoproterenol stimulated, yet high concentrations inhibited both primary and secondary glucose‐induced IRI responses. Prestimulation with either epinephrine or nor‐epinephrine, followed by replacement of the adrenergic agent with stimulating concentrations of glucose, produced a marked enhancement of the glucose‐induced primary response. This deferred enhancement was abolished by the further addition of either α or β receptor blocking agents during prestimulation. — These results suggests that adrenergic stimulation may both enhance and depress glucose‐stimulated IRI release and that the suppressive α‐type effect is exerted at a point distal to the enhancing β‐type effect in the chain of events leading to IRI release; that α and β types of effects are not mutualy exclusive; that adrenergic suppression of IRI release may act to ‘prime’ the B‐cell such that subsequent immediate responses become more marked. Since adrenergic ‘priming’ of B‐cells selectively affects the primary phase of glucose‐stimulated IRI release, the possibility that inadequate function of this priming mechanism may contribute to the delayed response in diabetes must be considered.