Autonomie ganglia may be regulated, in part, by nicotinic receptors. To test whether basal insulin secretion may be modulated by an endogenous pancreatic ganglionic mechanism, the effects of ganglionic pre- and postsynaptic nicotinic receptor antagonism were studied in the in vitro canine pancreas. Combined infusion of atropine, phentolamine, and propranolol had no affect on insulin secretion (P < .30). Presynaptic nicotinic receptor blockade by β-bungarotoxin (β-BuTX) in combination with atropine and phentolamine reduced mean insulin secretion (78 ± 18 U/ml, P < .0025) from preinfusion concentrations (287 ± 43 U/ml). The decrease in insulin secretion resulting from BuTX, atropine, and phentolamine was prevented by the addition of either specific postsynaptic nicotinic receptor blockade by α-bungarotoxin (P < .05) or propranolol (P < .005). Because it is known that postsynaptic nicotinic receptor agonism may stimulate the intragan-glionic release of norepinephrine, these results suggest that nicotinic receptors are present at the ganglionic level in the pancreas and modulate insulin secretion by a complex intraganglionic mechanism. The postulated ganglionic nicotinic receptor-mediated mechanism may operate by the interaction of a β-adrenergic inhibitory component, which may be activated by intraganglionic norepinephrine, and a stimulatory nonmuscar-inic nonadrenergic (possibly peptidergic) component, which may be activated in the absence of intraganglionic norepinephrine.

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