Rolo of NO as a causative factor for hypertensive cerebral injury

1998 Fiscal Year Final Research Report Summary

• Project/Area Number: 09670241
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Kinki University
• Principal Investigator: ITO Hiroyuki Research Institute of Hypertension, Kinki University Professor, 付置研究所, 教授 (60113148)
• Co-Investigator(Kenkyū-buntansha): TAKEMORI Kumiko School of Medicine, Pathology, Kinki University Assistant, 医学部, 助手 (00288888) ; KAWAI Jun School of Medicine, Pathology, Kinki University Lecturer, 医学部, 講師 (10234006) ; YAMAMOTO Kazuo Research Institute of Hypertension, Kinki University Assistant, 付置研究所, 助手 (40182612)
• Project Period (FY): 1997 – 1998
• Keywords: hypertensive cerebral injury / NO / free radical / adhesion molecule

Research Abstract

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.