Sweet C S, Gaul S L
Can J Physiol Pharmacol. 1977 Aug;55(4):968-71. doi: 10.1139/y77-132.
Methyldopate (methyldopa (ethyl ester)), carbidopa, clonidine, and ST-91 were evaluated for their effects on conditioned salivation in unanesthetized dogs. Clonidine produced dose-dependent inhibition of salivation 20 min after an intravenous injection. At equivalent and larger doses, ST-91, a clonidine analog which does not penetrate the blood-brain barrier, was ineffective in inhibiting conditioned salivation, suggesting that central rather than peripheral mechanisms are involved in clonidine-induced inhibition of salivation. Methyldopate also produced a dose-dependent inhibition of salivation in dogs. The mechanism involved in methyldopa-induced inhibition of salivation may involve both central and peripheral mechanisms because carbidopa, an inhibitor (like methyldopa) of peripheral aromatic decarboxylase (EC 4.1.1.28), significantly inhibited salivation.
对甲基多巴（甲基多巴乙酯）、卡比多巴、可乐定和ST - 91进行了评估，观察它们对未麻醉犬条件性唾液分泌的影响。静脉注射可乐定20分钟后，其对唾液分泌产生剂量依赖性抑制作用。在等效剂量及更大剂量时，ST - 91（一种不能穿透血脑屏障的可乐定类似物）对抑制条件性唾液分泌无效，这表明可乐定诱导的唾液分泌抑制涉及中枢而非外周机制。甲基多巴也对犬的唾液分泌产生剂量依赖性抑制作用。甲基多巴诱导唾液分泌抑制的机制可能涉及中枢和外周机制，因为外周芳香族脱羧酶（EC 4.1.1.28）的抑制剂卡比多巴（与甲基多巴类似）能显著抑制唾液分泌。
