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

Abstract

The cardiovascular responses to intravenous doses of 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. In contrast, inhibiting nigrostriatal dopamine pathways with SN lesions led to a significant reduction in the epinephrine-induced bradycardia. Furthermore, local injection of a dopamine receptor agonist apomorphine into the caudate-putamen complex (CP) facilitated reflex bradycardia, while intra-CP injection of dopamine antagonists such as haloperidol and pimozide inhibited it. Moreover, 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. Therefore, the present data indicate that a dopaminergic synapse occurs within the caudate-putamen complex which mediates reflex bradycardia in the rat. Key Words: dopamine receptor, caudate-putamen complex, reflex bradycardia, substantia nigra. Recent studies of the effects of dopamine (DA) and its agonists in the cardiovascular system have clearly demonstrated the potential of the dopaminergic system in regulating cardiovascular function. For example, dopamine or apomorphine given systemically causes peripheral vasodilatation (GOLDBERG et al., 1977 ; LIN et al., 1979) and reduction of arterial blood pressure (BOLME et al., 1977) which are competitively counteracted by pimozide (a DA receptor blocking agent). After intracisternal injection, apomorphine (a DA receptor-stimulating agent) caused increased arterial pressure in rats (BOLME et al., 1977). In addition, high levels of DA have been found in the carotid bodies of both rats and cats (HANBAUER, 1977; ZAPATA, 1977). However, to our knowledge, little information is available on the role played by the central dopaminergic system in the

Subtle Cardiovascular Dysfunction in the Unilateral 6-Hydroxydopamine-Lesioned Rat

“…Both studies suggest a relationship between the loss of DA in the striatum and the control of HR. Previous studies have found evidence to support a direct association between the nigrostriatal system and cardiovascular function [37–39]. Electrical [40] or chemical [41] stimulation of the SN pars compacta in rats enhanced DA release in the striatum and elicited proportional hypertension and tachycardia.…”