Cm. Castro et al., Proteoglycan production by vascular smooth muscle cells from resistance arteries of hypertensive rats, HYPERTENSIO, 34(4), 1999, pp. 893-896
Citations number
22
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Extracellular matrix (ECM) modifications in the vascular wall contribute to
the narrowing of arteries in hypertension. Because direct evidence for the
role of proteoglycans (PGs) in the pathological process of resistance-size
d arteries has not already been demonstrated, we examined the effect of gro
wth factors on secreted and membrane-bound PG synthesis by cultured mesente
ric vascular smooth muscle cells (VSMC) from spontaneously hypertensive rat
s (SHR) and Wister rats. After 48 hours of stimulation with angiotensin II
(Ang II), platelet-derived growth factor (PDGF-BB), and 10% fetal calf seru
m (FCS) or 0.1% FCS as control, PG synthesis (in dpm/ng DNA) was evaluated
in the medium (M-ECM) and in the cell layer (P-ECM) by a double-isotopic la
bel method with both [H-3]-glucosamine and [S-35]-sodium sulfate, which are
incorporated into all complex carbohydrates or only into sulfated disaccha
rides, respectively. VSMC from SHR displayed a significantly lower level of
synthesis of M-ECM [H-3]-PGs than those of Wistar rats in all the experime
ntal groups, including the control group (0.1% FCS), but no differences in
M-ECM [S-35] uptake were found in any case. In the P-ECM, Ang II was the on
ly factor that produced a lesser effect on [H-3]-glucosamine and a greater
effect on [S-35]-sodium sulfate uptakes in VSMC from SHR than from Wistar r
ats. The most prominent change seen in VSMC from SHR was an increased sulfa
tion, assessed by [S-35]/[H-3] ratio, in nonstimulated cells and in respons
e to 10% FCS and Ang II but not to PDGF-BB compared with VSMC from Wistar r
ats. These data indicate the existence of changes in PG modulation in the r
esistance vessels of SHR, which suggests that PGs may contribute to the dev
elopment of structural and functional modifications in hypertensive states.