Hata F, Ishida H, Kondo E
Br J Pharmacol. 1986 Nov;89(3):473-83. doi: 10.1111/j.1476-5381.1986.tb11147.x.
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.
在体外研究了多巴胺对大鼠腮腺组织淀粉酶分泌的影响。多巴胺以剂量依赖性方式诱导该组织显著分泌淀粉酶。其半数有效浓度（EC50）值约为4微摩尔，在浓度为100微摩尔时获得最大反应。多巴胺诱导的分泌受到多巴胺拮抗剂氟哌啶醇、（+）-丁酰苯和螺哌啶醇的抑制。阿托品显著降低多巴胺诱导的分泌，而毒扁豆碱增强分泌。对腺体进行副交感神经切除导致多巴胺诱导的分泌显著减少，但并未降低多巴胺与阿托品共同诱导的分泌。在已用[3H]-胆碱加载的组织制剂中研究了多巴胺诱导的乙酰胆碱（ACh）从组织中副交感神经末梢的释放。多巴胺引发对钙离子敏感的氚释放，多巴胺拮抗剂或副交感神经切除可阻止这种释放。对大鼠进行交感神经切除或利血平处理导致多巴胺诱导的分泌显著减少，但去甲肾上腺素（NA）或异丙肾上腺素诱导的分泌增加。通过用[3H]-NA预加载腮腺组织来研究多巴胺诱导的NA释放。多巴胺诱导对钙离子敏感的氚释放，多巴胺拮抗剂或交感神经切除可阻止这种释放。几条间接证据有力地表明，多巴胺在腮腺组织中有一个独立于NA受体的特定作用位点。在交感神经切除或利血平处理的腺体中，阿托品完全抑制多巴胺诱导的淀粉酶分泌，这表明多巴胺对突触后没有直接作用。这些发现表明，多巴胺分别通过从副交感神经和交感神经末梢释放的ACh和NA介导的两种间接方式诱导淀粉酶分泌。
