Abstract
Secretion of pancreatic enzymes is under control of both neural and hormonal factors with neural control exerted by cholinergic fibers running in both the vagus and splanchnic nerves (1). Cholinergic stimulation is blocked by atropine which, however, does not affect stimulation by the gastrointestinal hormone cholecystokinin-pancreozymin (2). Acetylcholine and various nonmetabolized analogs have also been shown to induce enzyme release in vitro with the stimulation blocked by atropine (3-7).
Adrenergic agents cause profound inhibition of pancreatic function in vivo associated with vasoconstriction (8, 9). In a recent in vitro study, isoproterenol was found to stimulate amylase release from perfused cat pancreas but the effect was blocked by atropine and was felt mediated by acetylcholine in a nonphysiological manner (10). Both cholinergic and adrenergic nerve endings are present in the exocrine pancreas but essentially all fibers directly innervating acinar cells are cholinergic (11, 12).
In the present work we have examined the effects of a number of cholinergic and adrenergic agonists on amylase release from mouse pancreas in vitro. We have specifically looked for the existence of nicotinic or adrenergic receptors affecting amylase release and compared the secretory response to commonly used cholinergic analogs in the same preparation.
Materials and methods. All studies were carried out using male White Swiss mice (18-22 g) which were fasted overnight prior to use. The pancreases were removed and incubated in Krebs-Henseleit bicarbonate (KHB) solution (at 37°) either in 25 ml Erlenmeyer flasks or by means of a super-fusion apparatus (13, 14). In experiments involving addition of catecholamines, ascorbic acid was added at a concentration of 0.5 mM to retard oxidation. In flask experiments each pancreas was divided into four or five 20-25 mg fragments while in superfusion experiments the fragments were split between two chambers.
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