F. Amenta et al., VASCULAR AND NEURONAL HYPERTENSIVE BRAIN-DAMAGE - PROTECTIVE EFFECT OF TREATMENT WITH NICARDIPINE, Journal of hypertension, 14, 1996, pp. 29-35
Aim The brain is sensitive to hypertension, which causes a variety of
vascular and neuronal cerebral changes. The present study was designed
to assess the effect of long-term treatment with the Ca2+ channel blo
cker nicardipine on intracerebral (intraparenchymal) arteries in spont
aneously hypertensive rats (SHR) by using microanatomical techniques a
ssociated with image analysis. The effects of hypertension and treatme
nt with nicardipine on nerve cells and glial fibrillary acid protein (
GFAP)-immunoreactive glial cells were also evaluated. Effects of nicar
dipine on blood pressure In SHR a significant increase in systolic blo
od pressure in comparison with age-matched normotensive Wistar-Kyoto (
WKY) rats was noticeable. Treatment with nicardipine significantly red
uced systolic pressure in the SHR. The media:lumen ratio and the thick
ness of the tunica media were increased in medium (diameter between 15
0 end 50 mu m) and small (diameter <50 mu m) intracerebral arteries. T
his phenomenon was accompanied by luminal narrowing. Treatment with ni
cardipine significantly reduced the thickness of the tunica media, the
media:lumen ratio and increased the luminal area, primarily at the le
vel of small pial arteries and of intracerebral arteries. Effects of n
icardipine in the brain In control SHR, the number of neurones in the
frontal and occipital cortex was reduced in comparison with normotensi
ve WKY rats. GFAP-immunoreactive astrocytes were increased in number (
hyperplasia) and in size (hypertrophy), both in the frontal cortex and
in the occipital cortex of control SHR In the CA, field of the hippoc
ampus, the number of neurones and their size were decreased in SHR in
comparison with normotensive WKY rats. Hyperplasia of GFAP-immunoreact
ive astrocytes of white matter and hypertrophy of those of grey matter
was also noticeable. No important changes were found in other portion
s of the hippocampus. Treatment with nicardipine increased the number
of neurones in the frontal cortex and in the occipital cortex of SHR a
nd countered hyperplasia and hypertrophy of GFAP-immunoreactive astroc
ytes. Moreover, it increased the number of neurones in the CA, field o
f the hippocampus and decreased the number and the size of astrocytes
of the white matter and grey matter, respectively. Conclusions These f
indings show that treatment of SHR with nicardipine significantly redu
ced systolic blood pressure and induced moderate vasodilation of both
extracerebral and intracerebral arteries regulating cerebrovascular re
sistance. The compound also countered some microanatomical changes occ
urring in the hypertensive brain. The frontal and occipital (visual) c
ortex and the CA, field of the hippocampus were the cerebral areas mor
e sensitive to treatment with nicardipine. This suggests that nicardip
ine induces moderate cerebrovascular dilation and exerts neuroprotecti
ve effects on SHR neurones. The possible relevance of the neuroprotect
ive actions of nicardipine in the hypertensive brain deserves to be ev
aluated in future studies. (C) Rapid Science Publishers