Langer S Z, Vidal M, Duval N
Clin Exp Hypertens A. 1987;9(5-6):837-51. doi: 10.3109/10641968709161453.
Stimulation by agonists of presynaptic dopamine receptors on nerve terminals of peripheral sympathetic neurons results in inhibition of norepinephrine release and a concomitant reduction of end organ responses to sympathetic nerve stimulation. These presynaptic dopamine receptors are of the DA-2 subtype and can be blocked selectively by the antagonist S-sulpiride. Presynaptic DA-2 receptors are the target of action of agonists with potential antihypertensive and bradycardic effects. Under control conditions exposure to S-sulpiride on its own does not enhance norepinephrine release. Following chronic treatment of cats with pargyline, S-sulpiride produced a small but significant increase in the electrically-evoked release of 3H-norepinephrine from perfused atrial slices. The possible involvement of peripheral presynaptic DA-2 receptors in the antihypertensive effects of monoamine oxidase inhibitors is discussed.
外周交感神经元神经末梢上的突触前多巴胺受体激动剂刺激会导致去甲肾上腺素释放受到抑制，同时终末器官对交感神经刺激的反应也会相应降低。这些突触前多巴胺受体属于DA - 2亚型，可被拮抗剂S - 舒必利选择性阻断。突触前DA - 2受体是具有潜在降压和心动过缓作用的激动剂的作用靶点。在对照条件下，单独使用S - 舒必利不会增强去甲肾上腺素的释放。在用帕吉林对猫进行慢性治疗后，S - 舒必利使灌注心房切片中电诱发的3H - 去甲肾上腺素释放量出现了小幅度但显著的增加。本文讨论了外周突触前DA - 2受体可能参与单胺氧化酶抑制剂的降压作用。
