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

Abstract

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.

The direct inhibition of pancreatic electrolyte secretion by noradrenaline in the isolated perfused cat pancreas.

“…Pearson & Singh (1983) have demonstrated an increase in amylase secretion following field stimulation of rat pancreatic fragments, a response abolished by propranolol. This work confirms that of Lingard & Young (1983) who also demonstrated that amylase secretion could be evoked in the isolated perfused rat pancreas by the fl-adrenergic agonist isoprenaline.…”

An In Vitro Evaluation of Adrenergic Action on Rat Pancreatic Amylase Secretion: Lack of Stimulatory Effect.

“…The present results clearly demonstrate that adrenergic stimulation does not affect pancreatic amylase secretion in contrast to previous studies (Lingard and Young, 1983;Pearson and Singh, 1983;Pearson et al, 1984). In view of the suggestion that adrenergic stimulation indirectly influence secretion via changes in pancreatic blood MacLachlin, 1917), we used dispersed pancreatic acini to assess direct involvement cf catecholamines in pancreatic amylase secretion.…”

“…Many studies have also been published on pancreatic amylase release in response to sympathomimetic drugs (Demol and Sarles, 1980;Furuta et al, 1978;Hubel, 1970;Pederson and Schultz, 1974;Raptis et al, 1973;Lingard and Young, 1983). Recently, Pearson et al, reported that stimulation of adrenergic receptor induced pancreatic amylase secretion in isolated segments of rat pancreas (Pearson and Singh, 1983;Pearson et al, 1984).…”

Beta-Adrenergic Inhibition of Pancreatic Secretion in Dogs

“…Propranolol blocked this inhibition and had no effect on the response to cholecystokinin. These observations suggest that (1) terbutaline inhibits pancreatic secretion by a beta-adrenergic mechanism and (2) the primary effect of terbutaline on canine exocrine pancreas is inhibition of water and bicarbonate secretion.Other investigators demonstrated beta-adrenergic in fluences on in vitro rat pancreatic secretion [1,2]. Addi tionally, we have shown that terbutaline, a beta-adrener gic agonist, inhibits in vivo canine pancreatic secretion evoked by cholecystokinin [3], secretin [4] and a liquid meal [5].…”