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.