Angiotensin protects cortical neurons from hypoxic-induced apoptosis via the angiotensin type 2 receptor.

Journal Article (Journal Article)

The effects of angiotensin on mouse cortical neuronal cultures exposed to chemical-induced hypoxia was investigated. Cultures exposed to 10 mM sodium azide for 5 min showed a 17% increase in apoptosis when assayed 24 h postinsult. The N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 blocked sodium azide-induced cell death suggesting that the NMDA receptor contributes to the mediated cell death. Pretreatment of cultured neurons with angiotensin decreased sodium azide-induced apoptosis by 94%. When the AT(1) receptor was blocked by its receptor antagonist, losartan, angiotensin activation of the AT(2) receptor completely inhibited sodium azide-induced apoptosis. Pretreatment of neurons with the AT(2) receptor antagonist PD123319 resulted in angiotensin reducing sodium azide-induced apoptosis by 48%. These results demonstrate that angiotensin can significantly attenuate sodium azide-induced apoptosis primarily through activation of the AT(2) receptor and suggests that angiotensin may have a protective role in neurons undergoing ischemic injury.

Full Text

Duke Authors

Cited Authors

  • Grammatopoulos, T; Morris, K; Ferguson, P; Weyhenmeyer, J

Published Date

  • March 28, 2002

Published In

Volume / Issue

  • 99 / 2

Start / End Page

  • 114 - 124

PubMed ID

  • 11978402

International Standard Serial Number (ISSN)

  • 0169-328X

Digital Object Identifier (DOI)

  • 10.1016/s0169-328x(02)00101-8


  • eng

Conference Location

  • Netherlands