Background: Abnormalities in cardiovascular structure e.g. LV hypertro
phy and thickening of vessels (elastic and peripheral arteries, veins)
are hallmarks of renal failure. Among other hormones parathyroid horm
one (PTH) has been shown to affect cardiac function and has also been
identified as a permissive factor for the activation of the cardiac in
terstitium leading to myocardial fibrosis. The present study was desig
ned to examine whether PTH was also permissive for intramyocardial art
eriolar wall thickening in an experimental model of renal failure. Mat
erial and methods: Sham operated or subtotally nephrectomized rats (SN
X) were parathyroidectomized (PTX) and received either saline or rat 1
,34 PTH by osmotic minipump. After perfusion fixation, intramyocardial
arterioles were assessed using stereological techniques (wall thickne
ss, wall/lumen ratio, minimal lumen diameter, length density). Results
: Wall thickness of intramyocardial arterioles was significantly highe
r in SNX than in sham-op controls. SNX-PTX animals receiving solvent d
id not differ from sham-op controls while SNX-PTX animals receiving PT
H had increased values which were comparable with those of SNX. In add
ition, PTH treated animals showed signs of marked vascular smooth-musc
le cell and endothelial cell activation. Conclusions: The data suggest
that intramyocardial arteriolar wall thickening in experimental renal
failure and probable changes of vessel architecture in renal insuffic
iency in general are dependent upon the permissive effect of PTH.