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Department of Pharmacology, University of Virginia, Charlottesville, Virginia 22908-0735
The rostral ventrolateral medulla
(RVLM) may play an important role in the sympatholytic and hypotensive
effects of clonidine. The present study examined which type of
presympathetic RVLM neuron is inhibited by clonidine, and whether the
adrenergic presympathetic RVLM neurons are essential for
clonidine-induced sympathoinhibition. In chloralose-anesthetized and
ventilated rats, clonidine (10 µg/kg iv) decreased arterial pressure
(116 ± 6 to 84 ± 2 mmHg) and splanchnic nerve activity
(93 ± 3% from baseline). Extracellular recording and
juxtacellular labeling of barosensitive bulbospinal RVLM neurons
revealed that most cells were inhibited by clonidine (26/28) regardless
of phenotype [tyrosine hydroxylase (TH)-immunoreactive cells: 48 ± 7%; non-TH-immunoreactive cells: 42 ± 5%], although the
inhibition of most neurons was modest compared with the observed sympathoinhibition. Depletion of most bulbospinal catecholaminergic neurons, including 76 ± 5% of the rostral C1 cells, by
microinjection of saporin anti-dopamine 
-hydroxylase into the
thoracic spinal cord (levels T2 and T4, 42 ng · 200 nl
1 · side1) did not alter the
sympatholytic or hypotensive effects of clonidine. These data show that
although clonidine inhibits presympathetic C1 neurons, bulbospinal
catecholaminergic neurons do not appear to be essential for the
sympatholytic and hypotensive effects of systemically administered
clonidine. Instead, the sympatholytic effect of clonidine is likely the
result of a combination of effects on multiple cell types both within
and outside the RVLM.
rostral ventrolateral medulla; anti-dopamine -hydroxylase
saporin; splanchnic nerve activity; tyrosine hydroxylase; phenylethanolamine-N-methyl transferase
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