Mechanisms underlying the cardiovascular responses to spinal dopamine receptor stimulation by apomorphine in...

The present study investigated the mechanisms by which intrathecal (i.t.) apomorphine affects mean aortic pressure and heart rate in anesthetized rats. In saline-pretreated rats, upper thoracic (T2-T4) i.t. administration of apomorphine (48 microg/rat) induced immediate and significant hypotension and bradycardia. These responses were unaffected by intravenous (i.v.) methylatropine (1 mg/kg) or bilateral vagotomy, while they were prevented by i.t. lidocaine (25 microl at 1%) or i.v. hexamethonium (30 mg/kg). However, i.v. atenolol (1.5 mg/kg) suppressed the apomorphine-induced bradycardia without affecting the hypotension in either intact or bivagotomized rats. Bilateral adrenalectomy had no effect upon both maximal hypotensive and bradycardic responses to apomorphine (48 microg/rat at the T9-T10 level). These results suggest that hypotensive and bradycardic responses to i.t. apomorphine are due to an action in the spinal cord, presumably on sympathetic preganglionic neurons. These responses are dissociated and seem to result from withdrawal of sympathetic outflow to the vasculature and to the heart, respectively.