Activation of dopaminergic receptors within the caudate-putamen complex facilitates reflex bradycardia in the rat.

Abstract

The cardiovascular responses to i.v. epinephrine were assessed in sham-operated, substantia nigra (SN)-lesioned, and SN-stimulated rats under urethane anesthesia. Activation of nigrostriatal dopamine pathways with SN stimulation, although showing no alteration in the epinephrine-induced hypertension, did produce a significant enhancement in reflex bradycardia compared to the controls. Inhibiting nigrostriatal dopamine pathways with SN lesions led to a significant reduction in the epinephrine-induced bradycardia. Local injection of a dopamine receptor agonist apomorphine into the caudate-putamen (CP) facilitated reflex bradycardia, while intra-CP injection of dopamine antagonists such as haloperidol and pimozide inhibited it. The enhancement in the reflex bradycardia induced by intra-CP administration of apomorphine could readily be abolished by pretreatment with intra-CP administration of either haloperidol or pimozide. Apparently, a dopaminergic synapse occurs within the caudate-putamen complex which mediates reflex bradycardia in the rat.