Beta 1- and beta 2-adrenoceptor-mediated secretion of amylase from incubated rat parotid gland.

The present in vitro investigation was undertaken in an attempt to obtain further information on beta-adrenoceptor specificity and action in the rat parotid gland, with regard to amylase secretion. The beta 1-selective agonist prenalterol was roughly 800 times more potent than the beta 2-agonist terbutaline, and about 5 times more effective than noradrenaline in evoking amylase release . Propranolol was the most effective inhibitor of amylase release in all experiments. The beta 1-selective antagonist metoprolol and H104 /08 were also effective blockers of maximal noradrenaline- and prenalterol-induced release. The inhibition curves displayed biphasic shapes when amylase secretion was induced by noradrenaline, but not when prenalterol was the secretagogue. The beta 2-antagonist H35 /25 was without effect on maximal noradrenaline- and prenalterol-stimulated secretion. The amylase release evoked by submaximal concentration of terbutaline was inhibited by the two antagonists H35/25 and IPS 339. In another series of experiments propranolol and metoprolol clearly shifted the noradrenaline concentration-response curve to the right, whereas H35/25 was without effect. The results further demonstrate the major importance of the beta 1-adrenoceptor (noradrenaline-activated) in eliciting amylase release from the rat parotid gland. However, it is also suggested that the beta 2-adrenoceptors (terbutaline-activated) may to some extent serve the same function.