The aim of this study was to determine the phenotypic modulation in pr
eglomerular vascular smooth muscles and glomerular cells in hypertensi
on. Eight-week-old stroke-prone spontaneously hypertensive rats (SHRSP
) fed high sodium pellets (3%) were untreated or treated with a calciu
m antagonist, manidipine HCl (2 mg/kg per day), for 8 weeks. The expre
ssion of myosin heavy chain isoforms (MHC), SM2 (muscle-type) and SMem
b (non-muscle-type) or alpha-actin was examined by the immunohistochem
ical technique. In normotensive Wistar-Kyoto rats, both SM2 and alpha-
actin were expressed equally in the smooth muscles of preglomerular ve
ssels, and SMemb was expressed slightly in the glomerular epithelial c
ells. In the SHRSP, however, the expression of SM2 and alpha-actin was
significantly decreased or disappeared in the afferent arterioles, de
pending on the degree of vascular damage. In damaged glomeruli, SMemb
and alpha-actin were newly expressed in mesangial cells. Manidipine HC
l attenuated the renal damage and restored the expression of alpha-act
in in the afferent arterioles. There was a significant correlation bet
ween the glomerular damage and the attenuation of SM2 expression (r=0.
87). In conclusion, phenotypic modulation of vascular smooth muscles o
ccurred in hypertensive renal damage and was correlated with the glome
rular damage, where the phenotypic modulation also took place in the m
esangial cells. These results indicate that the phenotypic modulations
revealed by the expression of myosin isoforms might play an important
role in the development of hypertensive renal damage.