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Updated: Jul 14, 2025
2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia
Published on: June 22, 2013
Angiotensin II-mediated hippocampal hypoperfusion and vascular dysfunction contribute to vascular cognitive
Olivia Gannon1, Sarah M Tremble1, Conor McGinn1
1Department of Neurological Sciences, University of Vermont Larner College of Medicine, Burlington, Vermont, USA.
Insights
Chronic hypertension impairs memory by affecting hippocampal arterioles. Captopril treatment improved blood flow and memory in aged hypertensive rats, suggesting a therapeutic target.
Area of Science:
- Neuroscience
- Cardiovascular Science
- Gerontology
Background:
- Chronic hypertension is a major risk factor for vascular cognitive impairment (VCI).
- The specific mechanisms by which hypertension impacts hippocampal vasculature and contributes to VCI are not fully understood.
Purpose of the Study:
- To investigate the effects of hypertension on hippocampal arteriole (HA) function, hippocampal perfusion, and memory.
- To explore the role of angiotensin II signaling in hypertension-induced cognitive decline.
Main Methods:
- Studied memory, HA function, and perfusion in Wistar rats and spontaneously hypertensive rats (SHR) at different ages.
- Treated aged SHR with captopril or apocynin to assess therapeutic effects.
Main Results:
- Aged SHR exhibited impaired memory, HA endothelial dysfunction, and reduced hippocampal blood flow (~50%).
- Captopril treatment improved HA function, restored perfusion, and rescued memory in aged SHR.
- Apocynin treatment did not yield significant improvements.
Conclusions:
- Hippocampal vascular dysfunction, driven by angiotensin II signaling, contributes to memory decline in hypertension.
- Targeting hippocampal arterioles offers a potential therapeutic strategy for preserving neurocognitive health in aging hypertensive individuals.
Introduction:
Chronic hypertension increases the risk of vascular cognitive impairment (VCI) by ∼60%; however, how hypertension affects the vasculature of the hippocampus remains unclear but could contribute to VCI.
Methods:
Memory, hippocampal perfusion, and hippocampal arteriole (HA) function were investigated in male Wistar rats or spontaneously hypertensive rats (SHR) in early (4 to 5 months old), mid (8 to 9 months old), or late adulthood (14 to 15 months old). SHR in late adulthood were chronically treated with captopril (angiotensin converting enzyme inhibitor) or apocynin (antioxidant) to investigate the mechanisms by which hypertension contributes to VCI.
Results:
Impaired memory in SHR in late adulthood was associated with HA endothelial dysfunction, hyperconstriction, and ∼50% reduction in hippocampal blood flow. Captopril, but not apocynin, improved HA function, restored perfusion, and rescued memory function in aged SHR.
Discussion:
Hippocampal vascular dysfunction contributes to hypertension-induced memory decline through angiotensin II signaling, highlighting the therapeutic potential of HAs in protecting neurocognitive health later in life.
Highlights:
Vascular dysfunction in the hippocampus contributes to vascular cognitive impairment. Memory declines with age during chronic hypertension. Angiotensin II causes endothelial dysfunction in the hippocampus in hypertension. Angiotensin II-mediated hippocampal arteriole dysfunction reduces blood flow. Vascular dysfunction in the hippocampus impairs perfusion and memory function.
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