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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Original Contributions| August 01 1986
Modulation of Insulin Secretion by Pancreatic Ganglionic Nicotinic Receptors
John I Stagner;
Address correspondence to John Stagner, Ph.D., Research Service, VA Medical Center, 800 Zorn Avenue, Louisville, KY 40202.
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John I Stagner, Ellis Samols; Modulation of Insulin Secretion by Pancreatic Ganglionic Nicotinic Receptors. Diabetes 1 August 1986; 35 (8): 849–854. https://doi.org/10.2337/diab.35.8.849
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