Postsynaptic spinal alpha-adrenoceptors mediate effects of intrathecal clonidine

The cardiovascular effects of intrathecal administration of clonidine were examined after depletion of spinal cord noradrenaline or 5-hydroxytryptamine by pretreatment with 6-hydroxydopamine or 5,6-dihydroxytryptamine. Despite marked reduction in spinal noradrenaline or 5-hydroxytryptamine levels, resting blood pressure and heart rate were unchanged and the clonidine-induced hypotension and bradycardia were unimpaired. The results suggest that intrathecal clonidine acts via inhibitory spinal alpha-adrenoceptors located postsynaptically on the preganglionic nerve cell bodies.