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采用侧脑室微最注射法证明,谷氯酸受体哑型激动剂红藻氨酸(KA)可依剂量性地升高大鼠血压和加快心率。预先给予GABA合成抑制剂氮基脲140 mg/kg ip或GABA拮抗剂印防己毒1 mg/kg iv均可明显增强KA的作用;而GABA转氨酶抑制剂氨氧乙酸25μg/rat icv明显减弱KA的作用。结果表明,脑内GABA能神经元功能受抑,KA的中枢性心血管效应增强。从而推测,脑内GABA能神经元与谷氯酸能神经元之间相互制约,共同参与中枢性调节心血管的活动。
Microinjection of the lateral ventricle was used to demonstrate that KA, a kappa-dull agonist, increased blood pressure and increased heart rate in a dose-dependent manner. Pretreatment with GABA inhibitor, 180 mg / kg ip, or GABA antagonist, 1 mg / kg iv, significantly increased the effect of KA, whereas GABA aminotransferase 25 μg / rat icv significantly attenuated KA effect. The results showed that GABAergic neurons in the brain were inhibited and the central cardiovascular effects of KA were enhanced. It is speculated that brain GABAergic neurons and glutamatergic neurons in each other between the constraints and participate in the central regulation of cardiovascular activity.