Cognitive impairment, an underappreciated consequence of hypertension, is linked to cerebral arteriolar disease through poorly defined mechanisms. A study by Faraco et al. in this issue of the
D.G. Harrison, Tomasz J. Guzik
Proposed role of PVMs in cognitive dysfunction.
Hypertension leads to disruption of the blood-brain barrier, allowing Ang II and probably other neurohumoral agents to stimulate the production of ROS, including superoxide (O2.–), by PVMs. Superoxide and other ROS promote vasoconstriction, endothelial dysfunction, and oxidative injury in cerebral arterioles. These events cause dysfunction of the NVU, leading to cognitive impairment. AT1R, AT1 receptor; BBB, blood-brain barrier.