Description
In hypertension, abnormal regulation of microcirculation and endothelial dysfunction enhances vulnerability to hypertensive brain damage. In addition to lowering blood pressure, blockade of Angiotensin II AT1 receptors protects against stroke and stress in different animal models and this treatment may be of therapeutic advantage. We studied gene expression using Affymetrix Rat Genome U34A arrays from brain microvessels of spontaneously hypertensive rats (SHR) and their normotensive Wistar Kyoto controls (WKY) rats treated with an AT1 antagonist (candesartan, 0.3 mg/kg/day) or vehicle via osmotic minipumps for 4 weeks.