Korczyn A D, Keren O
Experientia. 1982 Apr 15;38(4):481-2. doi: 10.1007/BF01952650.
Injection of L-dopa in mice produces dose-dependent mydriasis. Pre-treatment with peripheral dopa-decarboxylase inhibitors (carbidopa and benserazide) or with an alpha-adrenergic blocking agent (phentolamine) abolishes the pupillary dilation caused by L-dopa. Pretreatment with fusaric acid, an inhibitor of dopamine-beta-hydroxylase, also antagonizes the mydriatic effect of L-dopa. Thus, our results suggest that the mydriasis produced in mice following the injection of L-dopa is caused by its peripheral conversion to noradrenaline, which stimulates alpha-adrenergic receptors in the dilator iridis. There was no evidence that stimulation of specific dopaminergic receptors was involved.
给小鼠注射左旋多巴会产生剂量依赖性瞳孔散大。用外周多巴脱羧酶抑制剂(卡比多巴和苄丝肼)或α-肾上腺素能阻断剂(酚妥拉明)进行预处理可消除左旋多巴引起的瞳孔扩张。用多巴胺-β-羟化酶抑制剂富马酸进行预处理也可拮抗左旋多巴的散瞳作用。因此,我们的结果表明,注射左旋多巴后小鼠出现的瞳孔散大是由其在外周转化为去甲肾上腺素所致,去甲肾上腺素刺激虹膜开大肌中的α-肾上腺素能受体。没有证据表明涉及特定多巴胺能受体的刺激。