Previously [Histochem J 1997;29:279-286], we found that
sympathectomy induced
neointima formation in ear but not cerebral arteries of genetically hyperlipidemic rabbits. To clarify the influence of sympathetic nerves in
atherosclerosis, and whether their influence involves vascular NO activity, we studied groups of normocholesterolemic intact (NI) and sympathectomized (NS), and hypercholesterolemic intact (HI) and sympathectomized (HS) rabbits (diet/
6-hydroxydopamine for 79 days). Segments of basilar (BA) and femoral (FA) arteries were studied histochemically, to evaluate differentiation (anti-
desmin, anti-
vimentin, anti-h-
caldesmon, and nuclear
dye), by confocal microscopy, and by in vitro myography. In BAs, staining of NI and NS groups was similar. In hypercholesterolemic groups, a small
neointima developed, more frequently in HS segments where smooth muscle cells (SMCs) positive for all
antibodies appeared to be migrating into the
neointima. In FAs, SMCs stained for the three
antibodies in the NI group, but we observed
desmin- and h-
caldesmon-negative,
vimentin-positive cells in some external medial layers of the NS, HI and HS groups, identical to adventitial fibroblasts. Large
neointimas of the HS group contained
vimentin-positive and largely
desmin- and h-
caldesmon-negative cells. Relaxation of BA or FA segments to
acetylcholine was not decreased by
sympathectomy.
Sympathectomy increased the contraction of resting FAs to nitro-
L-arginine (p = 0.0379). Thus,
sympathectomy aggravates the tendency for FA SMCs to migrate and dedifferentiate, increasing atherosclerotic lesions, without decreasing NO activity, but has only minor effects on BAs.