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对戊巴比妥钠麻醉家兔,静脉注射α-肾上腺素能受体拮抗剂育亨宾(Yohimbine)或γ-氨基丁酸(GABA)受体拮抗剂苦味毒(picrotoxin)均可明显对抗侧脑室注射氯压定(clonidine)的降血压作用。但是育亨宾不能阻断侧脑室注射GABA的中枢降压作用,而苦味毒则能完全阻断其降压效应。 家兔经GABA合成抑制剂氨基脲(Semicarbazide)静脉注射予处理后,动物于给药后3～4小时出现强烈惊厥,说明脑内GABA已降低到一定水平。此时用局部麻醉剂及肌松剂处理,在人工呼吸情况下,氯压定静脉注射的降压作用比不给氨基脲予处理的对照组动物显著减弱。 以上结果启示,中枢肾上腺素能受体激动而产生的降压作用有可能是通过GABA能抑制性神经元而实现。
In pentobarbital anesthetized rabbits, intravenous injection of Yohimbine, an alpha-adrenergic receptor antagonist, or picrotoxin, a gamma-aminobutyric acid (GABA) receptor antagonist, Intraventricular injection of clonidine (clonidine) hypotensive effect. However, yohimbine can not block the intracerebroventricular injection of GABA central antihypertensive effect, while the bitter virus can completely block its antihypertensive effect. After rabbits were treated with intravenous injection of Semicarbazide, a GABA synthesis inhibitor, the animals developed severe convulsions 3 to 4 hours after the administration, indicating that the brain GABA has been reduced to a certain level. At this point with local anesthetics and muscle relaxants in the case of artificial respiration, antihypertensive effect of intravenous injection of chlorine pressure than the semicarbazide-treated control animals significantly weakened. These results suggest that the central adrenergic receptor agonist and antihypertensive effect may be achieved through GABA inhibitory neurons.