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Dopamine‐induced amylase secretion from rat parotid salivary gland in vitro : an effect mediated via noradrenergic and cholinergic nerves.
Author(s) -
Hata Fumiaki,
Ishida Hajime,
Kondo Etsuo
Publication year - 1986
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1986.tb11147.x
Subject(s) - dopamine , endocrinology , medicine , reserpine , dopaminergic , chemistry , secretion , catecholamine , biology
1 The effect of dopamine on amylase secretion by rat parotid tissue was examined in vitro.2 Dopamine induced marked amylase secretion from the tissue in a dose‐dependent manner. Its EC 50 value was about 4 μM and the maximal response was obtained at a concentration of 100 μM. 3 The dopamine‐induced secretion was inhibited by the dopamine‐antagonists haloperidol, (+)‐butaclamol and spiroperidol. 4 Atropine reduced the dopamine‐induced secretion significantly, and physostigmine enhanced the secretion. 5 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. 6 Dopamine‐induced ACh release from parasympathetic nerve terminals in the tissue was studied in tissue preparations that had been loaded with [ 3 H]‐choline. Dopamine elicited Ca 2+ ‐sensitive tritium release, and dopamine antagonists or parasympathectomy prevented this release. 7 Sympathectomy or reserpine treatment of rats resulted in significant decrease in the dopamine‐induced secretion, but increase in noradrenaline (NA)‐ or isoprenaline‐induced secretion. 8 Dopamine‐induced NA release was studied by preloading the parotid tissue with [ 3 H]‐NA. Dopamine induced Ca 2+ ‐sensitive tritium release, and dopamine antagonists or sympathectomy prevented the release. 9 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. 10 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. 11 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.