Parkinson's disease has been described as a multisystem disorder that
includes alterations in the function of the autonomic nervous system.
The activity of the adrenal medulla in this disease has not been thoro
ughly investigated. Previous reports are reviewed that demonstrate tha
t the adrenal medullae of parkinsonian patients are compromised, havin
g a decreased content of all catecholamines and several neuropeptides.
An animal model was used to investigate whether the observations made
in human patients were related to extended treatment with antiparkins
onian medications or were a natural concomitant of the disease. Admini
stration of L-dopa and/or carbidopa to C57BL mice for 4-16 weeks had n
o significant effect on the level of any of the adrenal medullary cate
cholamines. Treatment with MPTP 4-16 weeks prior to sacrifice did not
deplete adrenal medullary catecholamines in these animals, thus not fu
lly mimicking Parkinson's disease in this animal model. The only signi
ficant effect was an interaction between group (MPTP or control) and t
reatment with antiparkinsonian medications; L-dopa, in the absence and
presence of carbidopa, had opposite effects in the two groups. Based
primarily on the lack of effect of antiparkinsonian medications on adr
enal medullary catecholamines, it was concluded that the adrenal medul
lary depletion observed in human patients was a peripheral concomitant
of Parkinson's disease. (C) 1994 Wiley-Liss, Inc.