Research ReportAngiotensin-(1-7) improves cognitive function in rats with chronic cerebral hypoperfusion

- Chronic cerebral hypoperfusion(CCH) was induced by the 2-vessel occlusion model.
- Angiotensin (1-7) significantly improved CCH-induced cognitive deficits.
- Angiotensin (1-7) increased hippocampal nitric oxide generation in CCH rats.
- Angiotensin (1-7) attenuated CCH-induced hippocampal neuronal death.
- Angiotensin (1-7) suppressed CCH-induced hippocampal astrocyte proliferation.

Chronic cerebral hypoperfusion (CCH) is associated with cognitive decline in aging, vascular dementia and Alzheimer׳s disease. Recently, angiotensin-(1-7) (Ang-(1-7)), one of the physiological constituents of the brain, was found to protect against cognitive dysfunction and brain ischemia. However, the effects of Ang-(1-7) on CCH-induced cognitive deficits remained unknown. In the present study, Ang-(1-7) significantly alleviated CCH-induced cognitive deficits in rats subjected to permanent bilateral occlusion of the common carotid arteries (a model of CCH). This neuroprotective effect was associated with increased nitric oxide generation, attenuated neuronal loss and suppressed astrocyte proliferation in the hippocampus. These findings demonstrate that Ang-(1-7) is a promising therapeutic agent for CCH-induced cognitive deficits.