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

Tom Grammatopoulos, Katherine Morris, Paul Ferguson, James Weyhenmeyer

Research output: Contribution to journalArticlepeer-review


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 AT1 receptor was blocked by its receptor antagonist, losartan, angiotensin activation of the AT2 receptor completely inhibited sodium azide-induced apoptosis. Pretreatment of neurons with the AT2 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 AT2 receptor and suggests that angiotensin may have a protective role in neurons undergoing ischemic injury.

Original languageEnglish (US)
Pages (from-to)114-124
Number of pages11
JournalMolecular Brain Research
Issue number2
StatePublished - Mar 28 2002


  • Angiotensin
  • Apoptosis
  • Cortical neuron
  • Hypoxia
  • NMDA
  • Primary culture

ASJC Scopus subject areas

  • Molecular Biology
  • Cellular and Molecular Neuroscience


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