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  • Title: Dopamine-induced amylase secretion from rat parotid salivary gland in vitro: an effect mediated via noradrenergic and cholinergic nerves.
    Author: Hata F, Ishida H, Kondo E.
    Journal: Br J Pharmacol; 1986 Nov; 89(3):473-83. PubMed ID: 2432981.
    Abstract:
    The effect of dopamine on amylase secretion by rat parotid tissue was examined in vitro. Dopamine induced marked amylase secretion from the tissue in a dose-dependent manner. Its EC50 value was about 4 microM and the maximal response was obtained at a concentration of 100 microM. The dopamine-induced secretion was inhibited by the dopamine-antagonists haloperidol, (+)-butaclamol and spiroperidol. Atropine reduced the dopamine-induced secretion significantly, and physostigmine enhanced the secretion. Parasympathectomy of the gland resulted in a significant decrease in the dopamine-induced secretion, but did not reduce the secretion induced by dopamine with atropine. Dopamine-induced ACh release from parasympathetic nerve terminals in the tissue was studied in tissue preparations that had been loaded with [3H]-choline. Dopamine elicited Ca2+-sensitive tritium release, and dopamine antagonists or parasympathectomy prevented this release. Sympathectomy or reserpine treatment of rats resulted in significant decrease in the dopamine-induced secretion, but increase in noradrenaline (NA)- or isoprenaline-induced secretion. Dopamine-induced NA release was studied by preloading the parotid tissue with [3H]-NA. Dopamine induced Ca2+-sensitive tritium release, and dopamine antagonists or sympathectomy prevented the release. Several lines of circumstantial evidence strongly suggested that dopamine has a specific site for action in the parotid tissue that is independent of NA receptors. In sympathectomized or reserpine-treated glands, atropine completely inhibited the dopamine-induced amylase secretion, suggesting that dopamine did not have a direct effect on postsynapses. These findings indicate that dopamine induces amylase secretion in two indirect ways mediated through ACh and NA released from parasympathetic and sympathetic nerve terminals, respectively.
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