Table 6.
Marker | Effect on BBB/consequences/contribution to risk of HT | References (for further reading) |
---|---|---|
Changes to the immune system and response | ||
Elevated levels of proinflammatory cytokines as TNF, IL-6, MCP-1, and sICAM-1 in the vasculature | Impact endothelial cell ability to regulate. Leukocyte interaction and infiltration, disruption of BBB | (80) |
Response to Angiotensin II due to chronic hypertension | ||
Increased MMP-9 and MMP-2 | Activated by the renin-angiotensin system in the vasculature, leading to vessel remodeling and disruption of the BBB | (81) |
Increase in serum PAI-1 | Activated by Angiotensin II, interferes with the tPa/alteplase degradation | (67) |
Increased ROS through NADPH oxidases | Macrophages in response to Angiotensin II Additionally, acute hypertension may attenuate the ability to cope with ROS | (82) |
Mechanical cellular changes due to chronic hypertension | ||
Remodeling of microvasculature: Decreased lumen diameter, increased vascular resistance, increased wall to lumen diameter. | Decreased endothelial cell function and reduced autoregulation ability | (80) |
BBB, Blood brain barrier; IL, interleukin; MCP-1, monocyte chemoattractant protein 1; NADPH, Nicotinamide adenine dinucleotide phosphate; PAI-1, plasminogen activator inhibitor-1; ROS, reactive oxygen species; sICAM, soluble intercellular adhesion molecule; TNF, tumor necrosis factor; tPa, tissue plasminogen activator.