Rolo of NO as a causative factor for hypertensive cerebral injury

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To elucidatc the role of NO as a causative factor for hypertensive cerebral injury, pathophysiological changes were investigated in stroke-prone SHR (SHRSP) cerebral cortex.(1)Edematosu changes and/or cerebral softening were found ini SI-IRSP cerebral cortex suffering from severe hypertension.(2)Immunohistochemical examination revealed increased expression of ICAM-1 (adhesion molecule of endothelial cells) and decreased expression of GLUT-1 (constitutive protein of blood=brain barrier) in such SHRSP brain.(3)Mac-1 (adhesion molecule in leukocytes) expression was much higher in SHRSP than in WKY.(4)Plasma NO metabolites content was higher in SHRSP.(5)iNOS expression in RT-PCR was also higher in SHRSP leukocytes.(6)These pathophysiological changes in SHRSP were enhanced by lipopolysaccharide (activation of leukocytes), but protected by S-mthylisothiourea (iNOS inhibitor).These results indicate the important role of NO generated by enhansed leukocyte-endothelial cell adhesion in hypertensive cerebral injury.