VASCULAR AND NEURONAL HYPERTENSIVE BRAIN-DAMAGE - PROTECTIVE EFFECT OF TREATMENT WITH NICARDIPINE

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