Struthers A D, Brown M J, Adams E F, Dollery C T
Br J Clin Pharmacol. 1985 Mar;19(3):311-7. doi: 10.1111/j.1365-2125.1985.tb02649.x.
The mechanism of the antihypertensive effect of alpha-methyldopa was compared with clonidine by administering equipotent single doses of clonidine (0.2 mg) and alpha-methyldopa (750 mg) to nine hypertensive patients. Plasma noradrenaline was followed for 8 h thereafter as an index of peripheral sympathetic activity. alpha-Methyldopa and clonidine produced the same hypotensive response at 6 and 8 h after dosing with a similar fall in plasma noradrenaline levels at these times. Linear regression analysis between the systolic blood pressure fall and the corresponding plasma noradrenaline fall, showed that the slopes of the two regression lines were similar for alpha-methyldopa as for clonidine. Equipotent doses of alpha-methyldopa and clonidine produce the same fall in plasma noradrenaline. This supports the current hypothesis that an alpha-methyldopa metabolite acts centrally, like clonidine, to reduce peripheral sympathetic activity.
通过给9名高血压患者服用等效单剂量的可乐定(0.2毫克)和α-甲基多巴(750毫克),比较了α-甲基多巴与可乐定的降压作用机制。此后,跟踪血浆去甲肾上腺素8小时,作为外周交感神经活动的指标。给药后6小时和8小时,α-甲基多巴和可乐定产生相同的降压反应,此时血浆去甲肾上腺素水平有相似程度的下降。收缩压下降与相应血浆去甲肾上腺素下降之间的线性回归分析表明,α-甲基多巴和可乐定两条回归线的斜率相似。等效剂量的α-甲基多巴和可乐定使血浆去甲肾上腺素产生相同程度的下降。这支持了当前的假说,即α-甲基多巴的一种代谢产物像可乐定一样,通过中枢作用来降低外周交感神经活动。