Studies on the cardiovascular actions of apomorphine in dogs: central versus peripheral mechanisms and role of the adrenal medulla.

The effects of apomorphine on blood pressure and heart rate were studied in normotensive chloralose anaesthetized dogs. Intravenous apomorphine (200 micrograms/kg) induced both a marked decrease of blood pressure and an increase in heart rate. These two cardiovascular responses to intravenous apomorphine were suppressed by haloperidol (1 mg/kg i.v.) or phentolamine (1 mg/kg i.v.). In contrast, pretreatment with atropine (1 mg/kg i.v.) only abolished the chronotropic (but not the hypotensive) response to apomorphine. Intravenous (500 micrograms/kg) but not intracisternal (50 micrograms/kg) domperidone suppressed the hypotensive responses elicited by intravenous or intracisternal apomorphine. In contrast, domperidone, injected either by intravenous or intracisternal route, abolished apomorphine-induced tachycardia. In adrenal demedullated dogs, the hypotensive response to apomorphine was abolished. These results suggest that the hypotensive response to apomorphine in normotensive dogs is mainly mediated by activation of peripheral dopaminergic mechanisms. The drug decreases blood pressure through stimulation of dopaminergic receptors located on sympathetic nerve terminals and on the adrenal medulla leading to a decrease of the release of catecholamines.