Matsumoto P, Brown A, Dunbar J C
Acta Diabetol Lat. 1984 Oct-Dec;21(4):333-40. doi: 10.1007/BF02582086.
Norepinephrine, dopamine and serotonin directly stimulated glucagon secretion by isolated perifused hamster islet. Propranolol blocked norepinephrine, dopamine and serotonin-stimulated glucagon release, suggesting that norepinephrine, dopamine and serotonin may modulate glucagon secretion via a beta-adrenergic mechanism. Dopamine and serotonin may exert their action directly via the beta receptor, stimulate residual adrenergic nerve terminals, or the release of other islet biogenic amines. We conclude that part of the stimulating effect of norepinephrine on glucagon release is beta adrenergically mediated and that dopamine and serotonin may affect glucagon secretion either directly or through the release of neurotransmitters that lead to glucagon release. Thus the intra-islet released dopamine and serotonin may contribute to the islets paracrine system by stimulating intra-islet adrenergic neurons.
去甲肾上腺素、多巴胺和5-羟色胺可直接刺激经分离并进行灌流的仓鼠胰岛分泌胰高血糖素。普萘洛尔可阻断去甲肾上腺素、多巴胺和5-羟色胺刺激的胰高血糖素释放,提示去甲肾上腺素、多巴胺和5-羟色胺可能通过β-肾上腺素能机制调节胰高血糖素分泌。多巴胺和5-羟色胺可能直接通过β受体发挥作用,刺激残留的肾上腺素能神经末梢,或释放其他胰岛生物胺。我们得出结论,去甲肾上腺素对胰高血糖素释放的部分刺激作用是由β-肾上腺素能介导的,多巴胺和5-羟色胺可能直接或通过释放导致胰高血糖素释放的神经递质来影响胰高血糖素分泌。因此,胰岛内释放的多巴胺和5-羟色胺可能通过刺激胰岛内肾上腺素能神经元而对胰岛旁分泌系统有贡献。