Goshima Y, Nakamura S, Misu Y
Department of Pharmacology, Yokohama City University School of Medicine, Japan.
Jpn J Pharmacol. 1990 Jan;52(1):174-7. doi: 10.1254/jjp.52.174.
In rat hypothalamic slices, antagonism by L-DOPA methyl ester and (-)-propranolol against L-DOPA-induced facilitation of endogenous noradrenaline (NA) release was characterized under the inhibition of dopadecarboxylase. L-DOPA at 10 nM to 1 microM facilitated the evoked NA release in a concentration-dependent manner. L-DOPA methyl ester (3, 10 and 30 nM) progressively shifted the concentration-release curve for L-DOPA to the right: Schild plots gave a straight line with a slope of 1.00 and pA2 was 8.9. This antagonistic action was not mimicked by L-phenylalanine, a substrate for L-DOPA transport system. In contrast, 10 and 100 nM propranolol concentration-dependently reduced the maximal effect of L-DOPA without rightward shift of the concentration-release curve. L-DOPA methyl ester is a potent competitive antagonist for the action of L-DOPA, and the recognition site of L-DOPA differs from presynaptic beta-adrenoceptors.
在大鼠下丘脑切片中，在多巴脱羧酶受到抑制的情况下，研究了L-多巴甲酯和（-）-普萘洛尔对L-多巴诱导的内源性去甲肾上腺素（NA）释放促进作用的拮抗作用。10 nM至1 μM的L-多巴以浓度依赖性方式促进诱发的NA释放。L-多巴甲酯（3、10和30 nM）使L-多巴的浓度-释放曲线逐渐右移：施尔德图给出一条斜率为1.00的直线，pA2为8.9。L-多巴转运系统的底物L-苯丙氨酸未模拟这种拮抗作用。相比之下，10和100 nM普萘洛尔浓度依赖性地降低了L-多巴的最大作用，但浓度-释放曲线未右移。L-多巴甲酯是L-多巴作用的有效竞争性拮抗剂，且L-多巴的识别位点与突触前β-肾上腺素能受体不同。
