Cardiovascular Effects of Dopamine After Central Administration Into Conscious Cats

Abstract

Dopamine (30 and 45 μg) administered intracerebroventricularly (i.c.v.) to a group of 10 conscious normotensive cats caused dose‐related increases in blood pressure and heart rate. In 4 of these animals the initial cardiovascular stimulant effects of i.c.v. dopamine were followed by hypotension and bradycardia. α‐Methyldopamine (30 and 45 μg i.c.v.) produced qualitatively similar responses to dopamine except that the cardiovascular stimulant effects were smaller and the secondary depressant effects somewhat more prolonged. Both stimulant and depressant effects of i.c.v. dopamine and α‐methyldopamine were greatly inhibited by autonomic ganglion blockade or by adrenergic neurone blockade. The cardiovascular stimulant effects of both i.c.v. dopamine and i.c.v. α‐methyldopamine were selectively inhibited by β‐adrenoceptor blocking agents whilst the cardiovascular depressant effects of these substances were abolished by the α‐adrenoceptor blocker phentolamine or by the dopamine‐β‐hydroxylase inhibitor disulfiram. Haloperidol by either i.c.v. or the intravenous route abolished both cardiovascular stimulant and depressant effects of i.c.v. dopamine, whilst pimozide by either route inhibited only the cardiovascular stimulant effects. In 2 cats, injection of dopamine into the cisterna magna produced predominantly depressant effects on the cardiovascular system except with a higher dose which induced biphasic responses.

Central Effects of Dopamine and Bromocriptine on Vasopressin Release and Blood Pressure

“…Similar controversy exists with regard to the effects of centrally administered DA on blood pressure: there are reports that i.c.v. DA caused biphasic changes in blood pressure [9], decreased it [15], or was without effect [16].…”

“…Although in these circum stances it is difficult to determine the true role of dopaminergic neurons in the control of vasopressin release, there is some reason to believe that this role may be expressed by the actions of BC under the present experimental conditions. It is well known that central dopaminergic neurons terminate in the supraoptic nucleus, median eminence, and the neural lobe of the posterior pituitary [3, 30], and that the central administration of dopamine (DA) or the peripheral administration of L-dopa can affect the release of vasopres sin and have cardiovascular effects [ 1,2,4,9,15,16, 21,23, 25, 27, 29]. It is likely, therefore, that dopaminergic neurons participate in the control of vasopressin release and the re gulation of arterial blood pressure, and that the regulation of blood pressure may be mediated by changes in vasopres sin release and activity of the sympathetic nervous system.…”

Cardiovascular Responses Produced by the Injection of Dopamine Into the Cerebral Ventricles of the Unanaesthetized Dog

“…In the unanaesthetized cat, Day & Roach (1976) found that /-adrenoceptor antagonism with either intraventricular propranolol or alprenolol abolished the cardiovascular response to i.c.v. dopamine.…”

“…dopamine were followed by hypotension and bradycardia. It was suggested by Day & Roach (1976) that the secondary depressor effect was due to the conversion of some of the dopamine to noradrenaline, as this secondary response was abolished by an inhibitor of dopamine-f-hydroxylase, disulphiram, and by a-adrenoceptor blockade with phentolamine. However, no such cardiovascular depressant phase was observed in the dogs in our study.…”

“…In a recent study by Day & Roach (1976), the injection of dopamine into the cerebral ventricles of unanaesthetized cats caused an increase in blood pressure and heart rate. In some of the cats studied, the initial cardiovascular stimulant effects of i.c.v.…”