Abstract
Previous studies had shown an atropine sensitive, excitatory action of i.v. ethanol on pancreatic protein secretion in alcohol fed dogs and also an increased intrapancreatic acetylcholine activity. In an attempt to clarify these observations, the dose-inhibition effect of atropine, the dose-response effect of a cholinergic agonist and the effect of vagal stimulation on pancreatic protein output in alcoholic and normal dogs was compared. The inhibitory effect of atropine and the effect of vagal stimulation were unchanged but the sensitivity to exogenous cholinergic stimulation was decreased in alcoholic dogs compared to normals. It is suggested, that the chronic repetitive ethanol exposure of acinar muscarinic receptors, desensitizes them to cholinergic stimulation but induces paradoxical sensitivity to ethanol, while the interaction of atropine is left unchanged. The increased availability of acetylcholine would only be an adaptive phenomenon to the desensitization.