β1-and β2-adrenoceptor-mediated secretion of amylase from incubated rat parotid gland |
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Authors: | B CARLS
DANIELSSON R HENRIKSSON |
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Institution: | B. CARLSÖÖ,Å. DANIELSSON,R. HENRIKSSON |
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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. |
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Keywords: | at parotid gland amylase release β -adrenoceptor subtypes selective antagonists |
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