[The glial endothelin-nitric oxide system in ischemia-related neuronal cell death].
Both endothelin and nitric oxide (NO) have been proposed to act as pathophysiological factors in ischemia-related neural damage. This review is concerned with the participation of the glial endothelin-NO system in ischemia-related neuronal cell death. In the rat brain with cerebral apoplexy, endothelin, endothelin receptors and NO synthase (NOS) were rich in the glial cells of damaged brain areas. The brain subjected to transient forebrain ischemia contained astrocytic endothelins and microglial expressions of the ETB-receptor and NOS aggregating in the damaged CA1 subfield of the hippocampus at 7 days after the ischemia. Astrocytic endothelin, ETB-receptor and NOS became more apparent at 28 days after the ischemia, corresponding to a time when neural tissue-repair/remodeling after damage occurs, whereas no activities of the endothelin-NO system are observed in microglia. In the in vitro experiment, endothelin was found to modulate the release of NO from the hippocampal slices subjected to transient forebrain ischemia. There may be a cross-talk between the endothelin system and NO in the astrocytes and microglia during the process of ischemia-related neuronal cell death and neural tissue-remodeling.
Yamashita
K
K
Department of Pharmacology, Nagasaki University School of Medicine, Japan.
Sakurai-Yamashita
Y
Y
Niwa
M
M
Taniyama
K
K
D000818:Animals; D001253:Astrocytes / Q000502:physiology; D016923:Cell Death; D016232:Endothelins / Q000502:physiology*; D006624:Hippocampus / Q000378:metabolism; D006801:Humans; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D017628:Microglia / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D017466:Receptors, Endothelin / Q000378:metabolism
D016232:Endothelins; D017466:Receptors, Endothelin; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase