The role of the blood–brain barrier in hypertension

• Published in: Experimental physiology 2018-03, Vol.103 (3), p.337-342
• Main Authors: Setiadi, Anthony, Korim, Willian S., Elsaafien, Khalid, Yao, Song T.
• Format: Article
• Language: English
• Subjects: Angiotensin; Angiotensin II; Animals; Astrocytes; Autonomic nervous system; Autonomic Nervous System - metabolism; Biological Transport; Blood-brain barrier; Blood-Brain Barrier - metabolism; Brain - metabolism; Cardiovascular diseases; Central nervous system; Coronary artery disease; Cytokines; Health risk assessment; Heart diseases; Heart failure; Homeostasis; Humans; Hypertension; Hypertension - metabolism; Immune system; Inflammation; Leukocytes; Microglia; Molecular modelling; Reviews; sympathetic nervous system; Therapeutic applications
• ISSN: 0958-0670; 1469-445X
• DOI: 10.1113/EP086434

New Findings What is the topic of this review? This review highlights the importance of the blood–brain barrier in the context of diseases involving autonomic dysfunction, such as hypertension and heart failure. What advances does it highlight? It highlights the potential role of pro‐inflammatory cytokines, leucocytes and angiotensin II in disrupting the blood–brain barrier in cardiovascular diseases. Advances are highlighted in our understanding of neurovascular unit cells, astrocytes and microglia, with a specific emphasis on their pathogenic roles within the brain. The blood–brain barrier (BBB) is a crucial barrier that provides both metabolic and physical protection to an immune‐privileged CNS. The BBB has been shown to be disrupted in hypertension. This review addresses the importance of the BBB in maintaining homeostasis in the context of diseases related to autonomic dysfunction, such as hypertension. We highlight the potentially important roles of the immune system and neurovascular unit in the maintenance of the BBB, whereby dysregulation may lead to autonomic dysfunction in diseases such as heart failure and hypertension. Circulating leucocytes and factors such as angiotensin II and pro‐inflammatory cytokines are thought ultimately to downregulate endothelial tight junction proteins that are a crucial component of the BBB. The specific mechanisms underlying BBB disruption and their role in contributing to autonomic dysfunction are not yet fully understood but are a growing area of interest. A greater understanding of these systems and advances in our knowledge of the molecular mechanisms causing BBB disruption will allow for the development of future therapeutic interventions in the treatment of autonomic imbalance associated with diseases such as heart failure and hypertension.