Transient hypoxia/hypoglycemia upregulates endothelin B receptors in cultured rat astrocytes

✍ Scribed by Hirotomo Shibaguchi; Akihiko Himeno; Kazuto Shigematsu; Yasufumi Kataoka; Masami Niwa

• Book ID: 101259048
• Publisher: John Wiley and Sons
• Year: 2000
• Tongue: English
• Weight: 65 KB
• Volume: 31
• Category: Article
• ISSN: 0894-1491
• DOI: 10.1002/(sici)1098-1136(200007)31:1<91::aid-glia90>3.0.co;2-e

✦ Synopsis

Endothelins are potent vasoactive peptides that bind to their specific receptors, playing an important role in the CNS under physiological and pathophysiological conditions. Astrocytes, which have been shown to express these receptors, also have a considerable role to play under physiological and pathophysiological conditions, particularly those involved in delayed neuronal death. We carried out in vitro receptor autoradiographic binding experiments using specific ligands for endothelin receptors on cultured rat astrocytes. On astrocytes, the specific binding sites for 125 I-PD151242 (a selective endothelin A receptor antagonist) and 125 I-IRL 1620 (a selective endothelin B receptor agonist) were detected. We also characterized the qualitative and quantitative changes of endothelin receptors 24 h after subjecting cultured rat astrocytes to a transient 4-h hypoxia/hypoglycemia insult, used as a model of delayed neuronal death. After transient hypoxia/hypoglycemia, the number of endothelin B receptors increased significantly on cultured astrocytes, but this did not occur among the endothelin A receptors. These findings suggest that the astrocytic effects associated with endothelin in delayed neuronal death include gliosis or the repair process or both, manifested primarily by an increase in the number of endothelin B receptors. This rise does not require interaction with other types of CNS cells. Endothelin A receptors might have a role taking their number into consideration on rat astrocytes under both physiological and pathophysiological conditions. GLIA 31: 91-94, 2000.