Differences in dopamine- and noradrenaline-induced amylase release from the rat parotid gland

The effects of dopamine and noradrenaline on amylase secretion from rat parotid gland were studied in a batch incubation system. Dopamine effectively caused amylase secretion but the concentration-response curve was shifted to the right in reserpinized animals, suggesting a minor indirect component in the action of dopamine. The noradrenaline-evoked secretion was the same in reserpinized glands as in the controls. Bromocriptine, a dopamine receptor agonist, was without effect on amylase secretion. The dopamine receptor antagonists pimozide, chlorpromazine, haloperidol and droperidol as well as SKF 38393 all effectively inhibited dopamine-induced amylase secretion without affecting the enzyme release caused by noradrenaline. The D-2 antagonist sulpiride was without effect on both dopamine- and noradrenaline-stimulated secretion. The dopamine-induced secretion was also significantly blocked by the non-selective beta-blocker propranolol as well as by beta 1- and beta 2-selective antagonists. Several alpha-antagonists were all partial blockers of dopamine-stimulated amylase secretion. In contrast, the noradrenaline-evoked amylase release was exclusively abolished by propranolol and beta 1-selective antagonists. The results suggest that the dopamine- and noradrenaline-induced amylase secretion are activated via different receptor systems, and that dopamine stimulation is mainly a postsynaptic D-1 effect and only to a minor extent due to presynaptic interaction.