Szemeredi K, Pacak K, Kopin I J, Goldstein D S
Hypertension-Endocrine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
J Auton Nerv Syst. 1991 Sep;35(3):169-74. doi: 10.1016/0165-1838(91)90094-j.
Dihydroxyphenylalanine (DOPA) in plasma has been thought to originate from sympathetic nerve endings and to reflect catecholamine biosynthesis, because changes in DOPA levels follow pharmacologically- or environmentally-induced manipulations that alter turnover of the sympathetic neurotransmitter, norepinephrine (NE). Skeletal muscle may be an additional, non-neural source of circulating DOPA. In the present study we examined sympathoneural and skeletal muscle contributions to DOPA in arterial plasma in pithed rats. Electrical stimulation of the spinal cord causes discharges of sympathetic post-ganglionic neurons, with attendant release of NE into the bloodstream, and discharges of spinal motoneurons, which causes diffuse contraction of skeletal muscle. Stimulation of the spinal cord rapidly elevated arterial plasma concentrations of NE, dihydroxyphenylglycol (DHPG), and DOPA. Pre-treatment with curare, a skeletal muscle relaxant, did not affect the NE and DHPG responses but attenuated the DOPA responses by about 50%. Administration of chlorisondamine, a ganglionic blocker, abolished NE and DHPG responses to cord stimulation, and DOPA responses were decreased by about 90%. Adrenal-demedullation did not affect the stimulation-induced DOPA responses. The results demonstrate that in pithed rats undergoing spinal cord stimulation, DOPA is released into the bloodstream. Since this response is markedly inhibited after ganglionic blockade and also attenuated after skeletal muscle paralysis, the results provide indirect evidence that DOPA formed in sympathetic neurons can be stored in a non-neuronal pool and released during skeletal muscle contraction.
血浆中的二羟基苯丙氨酸（DOPA）一直被认为源自交感神经末梢并反映儿茶酚胺的生物合成，因为DOPA水平的变化与药理或环境诱导的操作相关，这些操作会改变交感神经递质去甲肾上腺素（NE）的周转。骨骼肌可能是循环DOPA的另一个非神经来源。在本研究中，我们检查了去大脑大鼠动脉血浆中交感神经和骨骼肌对DOPA的贡献。脊髓电刺激会导致交感神经节后神经元放电，随之NE释放到血液中，同时脊髓运动神经元放电，导致骨骼肌弥漫性收缩。脊髓刺激迅速升高了动脉血浆中NE、二羟基苯乙二醇（DHPG）和DOPA的浓度。用骨骼肌松弛剂箭毒预处理不影响NE和DHPG的反应，但使DOPA反应减弱约50%。给予神经节阻滞剂氯筒箭毒碱消除了NE和DHPG对脊髓刺激的反应，DOPA反应降低了约90%。肾上腺去髓质术不影响刺激诱导的DOPA反应。结果表明，在接受脊髓刺激的去大脑大鼠中，DOPA释放到血液中。由于这种反应在神经节阻断后明显受到抑制，在骨骼肌麻痹后也减弱，结果提供了间接证据，表明交感神经元中形成的DOPA可以储存在非神经元池中，并在骨骼肌收缩时释放。
