Zhang L, Zhang D S, Zhang S S
Department of Pharmacology, Zhangjiakou Medical College.
Yao Xue Xue Bao. 1991;26(6):411-4.
Microinjection of kainate (KA 0.125, 0.25, or 0.5 microgram), a special agonist for KA receptor, into rat lateral cerebral ventricle produced dose-dependent increases in blood pressure and heart rate. Pretreatment with semicarbazide (SCZ 140 mg/kg, ip), an inhibitor of GABA biosynthesis, or picrotoxin (PIC 1 mg/kg, iv), an antagonist for GABA, significantly enhanced the effects of KA on the cardiovascular system. These effects of KA were reduced by aminoxyacetic acid (AOAA 25 micrograms/rat, icv), an inhibitor of GABA aminotransferase. All these results described above imply that the function of GABA ergic neurons in brain can influence the effects of KA on the cardiovascular centre. We speculate that the central regulation of the cardiovascular system is involved in the interaction of GABA ergic neurons and glutamergic neurons in brain, thus, influencing the central sympathetic effects of efferent activity.
向大鼠侧脑室微量注射红藻氨酸(KA 0.125、0.25或0.5微克),一种KA受体的特殊激动剂,可使血压和心率呈剂量依赖性升高。用氨基脲(SCZ 140毫克/千克,腹腔注射),一种GABA生物合成抑制剂,或印防己毒素(PIC 1毫克/千克,静脉注射),一种GABA拮抗剂进行预处理,可显著增强KA对心血管系统的作用。KA的这些作用可被γ-氨基氧基乙酸(AOAA 25微克/大鼠,脑室内注射),一种GABA转氨酶抑制剂所减弱。上述所有这些结果表明,脑内GABA能神经元的功能可影响KA对心血管中枢的作用。我们推测,心血管系统的中枢调节涉及脑内GABA能神经元和谷氨酸能神经元的相互作用,从而影响传出活动的中枢交感效应。