Tachycardia, hypertension and decreased reflex bradycardia produced by striatal lesions induced by kainic acid.

The effects of intra-striatal injection of kainic acid on cardiovascular function were assessed in urethane-anesthetized rats. Intra-striatal administration of 2 micrograms of kainic acid (in a volume of 0.5 microliter) produced both tachycardia and hypertension. The tachycardia induced by intra-striatal injection of kainic acid was antagonized by either prior bilateral vagotomy or spinal transection of the animals (at C7). On the other hand, the hypertension induced by intra-striatal administration of kainic acid was antagonized by prior bilateral vagotomy, but not spinal transection. In addition, reflex bradycardia was produced by intravenous infusion of adrenaline in rats. Over the dose range (1.25-5.0 micrograms/kg, i.v.) of adrenaline used, a dose-dependent bradycardia was obtained. It was found that pretreatment of animals with intra-striatal injection of kainic acid, although causing no change in the adrenaline-induced pressor effect, did reduce the adrenaline-induced bradycardia. Intravenous administration of same dose of kainic acid had no effect on these cardiovascular responses. Thus, the data indicate that striatal neurones are involved in the central control of cardiovascular function.