Blair M L, Reid I A, Keil L C, Ganong W F
J Pharmacol Exp Ther. 1979 Sep;210(3):368-72.
When extracerebral dopa decarboxylase is inhibited by carbidopa, L-dopa lowers plasma renin activity (PRA). The present study was designed to determine whether this suppression of PRA is mediated by the sympathetic nerves, and to identify the peripheral adrenergic receptor types involved. All experiments were performed in pentobarbital-anesthetized dogs in which changes in renal perfusion pressure were minimized by means of a suprarenal aortic clamp. Neither alpha adrenoreceptor blockage with phenoxybenzamine nor beta adrenoreceptor blockade with propranolol was by itself sufficient to block the suppression of PRA by L-dopa with carbidopa. However, combined alpha and beta adrenoreceptor blockade lowered PRA and completely prevented any further suppression of PRA by L-dopa with carbidopa. It was also observed that phenoxybenzamine decreased PRA by 48% when administered to propranolol-treated animals. Taken together, these data indicate that L-dopa with carbidopa suppresses PRA by decreasing sympathetic nerve stimulation of both alpha and beta adrenoreceptors. Plasma vasopressin concnetration was significantly decreased by L-dopa with carbidopa both in the control group and in animals with combined alpha and beta adrenoreceptor blockade. Because plasma vasopressin levels decreased after L-dopa, vasopressin is unlikely to play a causative role in the suppression of PRA.
当脑外多巴脱羧酶被卡比多巴抑制时，左旋多巴会降低血浆肾素活性（PRA）。本研究旨在确定PRA的这种抑制作用是否由交感神经介导，并确定所涉及的外周肾上腺素能受体类型。所有实验均在戊巴比妥麻醉的犬身上进行，通过肾上主动脉夹将肾灌注压的变化降至最低。单独使用酚苄明阻断α肾上腺素能受体或普萘洛尔阻断β肾上腺素能受体本身都不足以阻止左旋多巴与卡比多巴对PRA的抑制作用。然而，联合阻断α和β肾上腺素能受体可降低PRA，并完全阻止左旋多巴与卡比多巴对PRA的进一步抑制。还观察到，给用普萘洛尔治疗的动物注射酚苄明时，PRA降低了48%。综上所述，这些数据表明，左旋多巴与卡比多巴通过减少对α和β肾上腺素能受体的交感神经刺激来抑制PRA。在对照组以及联合阻断α和β肾上腺素能受体的动物中，左旋多巴与卡比多巴均使血浆血管加压素浓度显著降低。由于左旋多巴后血浆血管加压素水平降低，血管加压素不太可能在PRA的抑制中起因果作用。
