β1‐and β2‐adrenoceptor‐mediated secretion of amylase from incubated rat parotid gland

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Abstract
The present in vitro investigation was undertaken in an attempt to obtain further information on β‐adrenoceptor specificity and action in the rat parotid gland, with regard to amylase secretion. The β1‐selective agonist prenalterol was roughly 800 times more potent than the β2‐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 β1‐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 β2‐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 β1‐adrenoceptor (noradrenaline‐activated) in eliciting amylase release from the rat parotid gland. However, it is also suggested that the β2‐adrenoceptors (terbutaline‐activated) may to some extent serve the same function.