Sabouni M H, Alkadhi K A, Lokhandwala M F
J Pharmacol Exp Ther. 1986 Jan;236(1):65-70.
Experiments were performed with fenoldopam (SKF-82526), a selective DA1 receptor agonist, and quinpirole (LY-171555), a selective DA2 receptor agonist, to determine their actions on ganglionic transmission. Fenoldopam caused significant inhibition of the tachycardia elicited during preganglionic stellate stimulation; however, it did not alter the positive chronotropic responses to postganglionic stellate stimulation, suggesting that the compound exerts its inhibitory action at the ganglia. Electrophysiological experiments in the isolated stellate ganglia showed that fenoldopam produced inhibition of ganglionic transmission as indicated by a significant reduction in the magnitude of the compound postganglionic action potential elicited during preganglionic nerve stimulation. The inhibition of ganglionic transmission produced by fenoldopam both under in vivo and in vitro conditions was antagonized by R-sulpiride and metoclopramide, but not by SCH 23390, S-sulpiride or phentolamine. Quinpirole produced significant inhibition of the tachycardia elicited during both preganglionic as well as postganglionic cardiac sympathetic nerve stimulation. This action of quinpirole was antagonized by RS-sulpiride. In electrophysiological experiments it was discovered that quinpirole caused a significant reduction in the magnitude of the compound action potential elicited during stimulation of preganglionic stellate nerve fibers. This inhibition of ganglionic transmission produced by quinpirole was antagonized by S- but not by R-sulpiride. Although phentolamine antagonized the inhibitory action of quinpirole, it was much less effective than S-sulpiride. Norepinephrine also produced inhibition of ganglionic transmission in the isolated stellate ganglia which was antagonized by phentolamine but not by S-sulpiride. These results demonstrate the presence of two subtypes of specific dopamine receptors in the stellate ganglia.(ABSTRACT TRUNCATED AT 250 WORDS)
使用选择性DA1受体激动剂非诺多泮（SKF - 82526）和选择性DA2受体激动剂喹吡罗（LY - 171555）进行实验，以确定它们对神经节传递的作用。非诺多泮可显著抑制节前星状神经节刺激期间诱发的心动过速；然而，它并未改变对节后星状神经节刺激的正性变时反应，这表明该化合物在神经节发挥其抑制作用。在分离的星状神经节中进行的电生理实验表明，非诺多泮可抑制神经节传递，这表现为在节前神经刺激期间诱发的复合节后动作电位幅度显著降低。非诺多泮在体内和体外条件下产生的神经节传递抑制作用，可被R - 舒必利和甲氧氯普胺拮抗，但不能被SCH 23390、S - 舒必利或酚妥拉明拮抗。喹吡罗可显著抑制节前和节后心脏交感神经刺激期间诱发的心动过速。喹吡罗的这一作用可被RS - 舒必利拮抗。在电生理实验中发现，喹吡罗可使节前星状神经纤维刺激期间诱发的复合动作电位幅度显著降低。喹吡罗产生的这种神经节传递抑制作用可被S - 舒必利而非R - 舒必利拮抗。尽管酚妥拉明可拮抗喹吡罗的抑制作用，但其效果远不如S - 舒必利。去甲肾上腺素也可在分离的星状神经节中抑制神经节传递，这可被酚妥拉明而非S - 舒必利拮抗。这些结果表明星状神经节中存在两种特定多巴胺受体亚型。（摘要截短于250字）
