EFFECTS OF DOPAMINE, APOMORPHINE, GAMMA-HYDROXYBUTYRIC ACID, HALOPERIDOL AND PIMOZIDE ON REFLEX BRADYCARDIA IN RATS

Abstract

The cardiovascular responses to i.v. doses of epinephrine were assessed in vehicle-controlled, dopamine-treated, apomorphine-treated, .gamma.-hydroxybutyric acid-treated, haloperidol-treated and pimozide-treated rats under urethan anesthesia. Previous exposure to several injections of epinephrine did not change the basal values of arterial pressure and heart rate. Dopaminergic transmission alterations within the brain did produce some influence on the reflex bradycardia in response to an elevation in arterial pressure. Blockade of dopaminergic receptors in brain with haloperidol or pimozide produced a significant reduction in reflex bradycardia compared to the controls. Direct activation of central dopamine receptors with dopamine and apomorphine or indirect activation of central dopamine receptors with .gamma.-hydroxybutyric acid led to an enhancement in epinephrine-induced bradycardia. Central dopamine systems play a role in the elaboration or modulation of reflex bradycardia. Brain dopamine appears to facilitate reflex bradycardia since activation of dopamine systems facilitated and blockade inhibited reflex bradycardia.