Angiotensin protects cortical neurons from hypoxic-induced apoptosis via the angiotensin type 2 receptor.
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.
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Related Subject Headings
- Vasodilator Agents
- Trypan Blue
- Sodium Azide
- Receptors, N-Methyl-D-Aspartate
- Receptors, Angiotensin
- Receptor, Angiotensin, Type 2
- Pyridines
- Neuroprotective Agents
- Neurons
- Neurology & Neurosurgery
Citation
Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Vasodilator Agents
- Trypan Blue
- Sodium Azide
- Receptors, N-Methyl-D-Aspartate
- Receptors, Angiotensin
- Receptor, Angiotensin, Type 2
- Pyridines
- Neuroprotective Agents
- Neurons
- Neurology & Neurosurgery