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beta-Adrenergic control of exocrine secretion by perfused rat pancreas in vitro.

To investigate the role of beta-adrenergic receptors in the genesis of pancreatic juice, we studied the effect of the agonist isoproterenol (25 or 2.5 mumol X 1(-1] on the isolated perfused rat pancreas and compared it with the effect of secretin (approximately 3 nmol X 1(-1). Isoproterenol stimulated flow of a HCO3-rich juice; the response was qualitatively similar to that evoked by secretin, but the flow rate was only about 70% of the maximum in vitro secretin response. We also studied the effects of the autonomic blockers propranolol, phentolamine, and atropine. None of the blockers altered basal pancreatic flow or the juice content of electrolytes or protein. The threshold for the response of the gland to isoproterenol was approximately 10 nmol X 1(-1), and effects appeared to be near maximal at approximately 1 mumol X 1(-1). As is the case with secretin stimulation in the rat, protein excretion was increased by isoproterenol in parallel with flow. However, juice potassium, which is increased by secretin, was not elevated. The effects of isoproterenol were antagonized by propranolol (25 mumol X 1(-1), and neither atropine nor atropine plus phentolamine had any effect on the gland response. We conclude that neither cholinergic nor adrenergic neurotransmitters are responsible for basal secretion. However, from the response of the gland to isoproterenol, it appears that stimulation of beta-adrenergic neural receptors is the counterpart to hormonal stimulation with secretin, just as activation of cholinergic receptors is to the actions of cholecystokinin.