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Evidence for a spinal site of action of clonidine on somatic and viscerosomatic reflex activity evoked on the pudendal nerve in cats.

Reflex activation of the pudendal nerve from bladder and urethral afferent fibers is believed to contribute to maintaining normal urinary continence under stress and to the pathophysiologic behavior seen in the urethral sphincter after suprasacral spinal cord injury. We sought to determine whether clonidine could influence, at a central level, somatic and viscerosomatic reflexes on the pudendal nerve independent of actions on the sympathetic nervous system. The expected central antisympathetic activity of clonidine could be demonstrated by near maximal lowering of the blood pressure at 5 micrograms/kg of clonidine. The drug had no influence on urethral constriction evoked by stimulation of the peripheral cut end of the pudendal nerve. However, central effects on the pudendal (somatic) nerve outflow could be demonstrated in both functional and electrophysiological experiments. Clonidine (5-50 micrograms/kg) inhibited the urethral constriction produced by stimulation of the central cut end of the pudendal nerve. Similarly, the compound action potentials recorded on the pudendal nerve in response to stimulation of the central cut end of the contralateral pelvic or pudendal nerves were reduced by as much as 75 to 85% by clonidine. The clonidine effect on the reflexes was resistant to acute transection of the spinal cord at T10; however, the antagonistic activity of prazosin was reduced dramatically. Yohimbine (0.5 mg/kg) but not prazosin (0.2 mg/kg) reversed the clonidine effect. There was no relationship between the action of clonidine on blood pressure and its action on the reflexes. We conclude that clonidine acts in the sacral spinal cord at alpha-2-adrenoceptors to depress a viscerosomatic and a somatic reflex associated with external urethral sphincter function.