ADRENERGIC MODULATION OF A SPINAL SYMPATHETIC REFLEX IN THE RAT

Patients with spinal cord injury involving transection of the lower ce rvical or upper thoracic spinal cord can experience an autonomic hyper reflexia characterized by exaggerated blood pressure increases in resp onse to visceral or somatic stimuli such as skin stimulation and urina ry bladder or rectal distention. These cardiovascular responses are me diated by activation of spinal sympathetic reflex (SSR) circuits in th e segments below the transection that are no longer controlled by thei r supraspinal inputs. We have examined the SSR in decerebrate, unanest hetized, paralyzed, artificially ventilated rats after acute spinal tr ansection in the sixth cervical segment and have determined its sensit ivity to i.v. administration of clonidine and other agents interacting with alpha-2 adrenergic receptors. The SSR amplitude, determined as t he area of the averaged excitatory potential evoked on the splanchnic sympathetic nerve by single stimuli (300 CLA) applied to the seventh t horacic dorsal root, was reduced to 14% +/- 6% of control with a cumul ative dose of clonidine of 27 mu g/kg. This inhibition was completely reversed by rauwolscine, idazoxan and RX821002, but not by prazosin. B oth guanabenz and UK-14304 also reduced the SSR amplitude (9% +/- 3% o f control at 0.4 mg/kg and 11% +/- 6% of control at 0.08 mg/kg, respec tively). 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 tr ansmission of information through SSR circuits after spinal cord injur y.