Adrenergic modulation of a spinal sympathetic reflex in the rat.

Patients with spinal cord injury involving transection of the lower cervical or upper thoracic spinal cord can experience an autonomic hyperreflexia characterized by exaggerated blood pressure increases in response to visceral or somatic stimuli such as skin stimulation and urinary bladder or rectal distention. These cardiovascular responses are mediated by activation of spinal sympathetic reflex (SSR) circuits in the segments below the transection that are no longer controlled by their supraspinal inputs. We have examined the SSR in decerebrate, unanesthetized, paralyzed, artificially ventilated rats after acute spinal transection in the sixth cervical segment and have determined its sensitivity to i.v. administration of clonidine and other agents interacting with alpha-2 adrenergic receptors. The SSR amplitude, determined as the area of the averaged excitatory potential evoked on the splanchnic sympathetic nerve by single stimuli (300 microA) applied to the seventh thoracic dorsal root, was reduced to 14% +/- 6% of control with a cumulative dose of clonidine of 27 micrograms/kg. This inhibition was completely reversed by rauwolscine, idazoxan and RX821002, but not by prazosin. Both guanabenz and UK-14304 also reduced the SSR amplitude (9% +/- 3% of control at 0.4 mg/kg and 11% +/- 6% of control at 0.08 mg/kg, respectively). These results indicate that activation of alpha-2 adrenergic receptors, within either the dorsal or intermediolateral horns of the spinal cord or within sympathetic ganglia, can significantly reduce transmission of information through SSR circuits after spinal cord injury.