Enhanced hypotensive response to intravenous apomorphine in chronic spinalized, conscious rats: role of spinal dopamine D(1) and D(2) receptors.
Intravenous (i.v.) treatment with apomorphine (0.3 mg/kg) in conscious rats with chronic spinal cord transection (at T5-T7) induced a significant hypotension, which was greater than that in sham-operated rats. The present study examined whether such an amplification results from an enhanced spinal dopamine D(1) and/or D(2) receptor-mediated depressor effect. Intrathecal (i.t.) pretreatment with domperidone (40 microg/rat at T9-T10), a dopamine D(2) receptor antagonist that does not cross the blood-brain barrier, blocked nearly 35 and 56% of the maximal apomorphine-induced hypotension in control and spinal rats, respectively. The remaining hypotension after i.v. domperidone (0.5 mg/kg) pretreatment (i.e. the spinal component of the response) was significantly greater in spinal rats than in controls. In the latter animals, apomorphine-induced hypotension was fully abolished by metoclopramide (5 mg/kg, i.v.). However, in spinal rats, the hypotension was only abolished by combined pretreatment with i.v. metoclopramide and i.t. SCH 23390 (27 microg/rat at T9-T10). The results suggest that the enhancing hypotensive effects of i.v. apomorphine by spinal cord section are related to increased spinal dopamine D(1) and D(2) receptor-mediated depressor effects.[1]References
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