2005 Fiscal Year Final Research Report Summary

Candesartan Reduces Superoxide Production after Global Cerebral Ischemia

Research Project

Project/Area Number	16591428
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Cerebral neurosurgery
Research Institution	Akita University
Principal Investigator	SUGAWARA Taku Akita University, School of Medicine, Assistant Professor, 医学部, 講師 (80241660)
Co-Investigator(Kenkyū-buntansha)	KINOUCHI Hiroyuki Yamanashi University, School of Medicine, Professor, 大学院・医学工学総合研究部, 教授 (30241623)
Project Period (FY)	2004 – 2005
Keywords	global cerebral ischemia / superoxide / angiotensin receptor / angiotensin II
Research Abstract	Excessive superoxide production after cerebral ischemia is known to mediate neuronal injury. Angiotensin II type 1 receptor (AT1R) activation is recently identified as a source of superoxide, however, it has not been clear whether blockade of AT1R leads to reduction of superoxide and subsequent neuronal injury after ischemia. Normotensive rats received AT1R blocker, candesartan or vehicle and subjected to global cerebral ischemia. Candesartan rescued approximately 30% of the hippocampal CA1 neurons, whereas only 2% of neurons survived in vehicle-treated animals. There was significantly less superoxide production in these vulnerable neurons in candesartan-treated animals than in vehicle-treated animals. AT1R may play a pivotal role in superoxide production and subsequent injury in the vulnerable neurons after global cerebral ischemia.

(4 results)