title: Dopamine-induced amylase secretion from rat parotid salivary gland in vitro: an effect mediated via noradrenergic and cholinergic nerves.
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.
mesh_terms: D000681:Amylases / Q000378:metabolism*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002794:Choline / Q000378:metabolism; D004298:Dopamine / Q000494:pharmacology*; D018492:Dopamine Antagonists; D066298:In Vitro Techniques; D008297:Male; D009638:Norepinephrine / Q000378:metabolism; D010275:Parasympathetic Nervous System / Q000502:physiology*; D010306:Parotid Gland / Q000201:enzymology* / Q000294:innervation; D010830:Physostigmine / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012110:Reserpine / Q000494:pharmacology; D013562:Sympathectomy; D013564:Sympathetic Nervous System / Q000502:physiology*
chemical_list: D018492:Dopamine Antagonists; D001285:Atropine; D012110:Reserpine; D010830:Physostigmine; D000681:Amylases; D002794:Choline; D004298:Dopamine; D009638:Norepinephrine