Neuropsychiatry
By Randolph B. Schiffer, Stephen M. Rao, Barry S. FogelThe SNS may elicit different, and often opposing functions at different anatomic sites. Localized denervation of draining lymph nodes, with sparing of the nerves innervating the joint, exacerbated joint pathology, but sympathetic removal of sympathetic input, either by beta-AR blockade or chemical sympathectomy with 6-OHDA or guanethidine reduced arthritic symptoms. These results suggest that noradrenergic innervation of draining lymph nodes inhibits the generation of antigen-specific T cells but promotes inflammation of the joints. A similar complexity was demonstrated after beta-agonist administration. Administration of a high dose of EPI reduced the severity of experimental arthritis by an alpha2-AR-mediated mechanism, but a low dose of EPI exacerbated joint injury. These results indicate that care must be used in manipulating the SNS therapeutically in complex diseases.
The SNS may also influence autoimmune processes in humans. Alterations in autonomic activity have been reported in RA and MS, but it is not known whether these changes are induced in response to disease or whether alterations in the SNS play a role in initiating the disease. In children with juvenile RA, increased sympathetic activity and autonomic hyporesponsiveness were associated with disease exacerbation.
Published 2003
Lippincott Williams
& Wilkins