Open AccessBrain angiotensin converting enzyme-2 in central cardiovascular regulation
Author(s) -
Mazher Mohammed,
Clara Berdasco,
Eric Lazartigues
Publication year - 2020
Publication title -
clinical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.91
H-Index - 138
eISSN - 1470-8736
pISSN - 0143-5221
DOI - 10.1042/cs20200483
Subject(s) - central nervous system , renin–angiotensin system , angiotensin converting enzyme 2 , homeostasis , angiotensin ii , neuroscience , receptor , angiotensin ii receptor type 1 , effector , biology , sympathetic nervous system , endocrinology , medicine , blood pressure , microbiology and biotechnology , disease , covid-19 , infectious disease (medical specialty)
The brain renin-angiotensin system (RAS) plays an important role in the regulation of autonomic and neuroendocrine functions, and maintains cardiovascular homeostasis. Ang-II is the major effector molecule of RAS and exerts most of its physiological functions, including blood pressure (BP) regulation, via activation of AT1 receptors. Dysregulation of brain RAS in the central nervous system results in increased Ang-II synthesis that leads to sympathetic outflow and hypertension. Brain angiotensin (Ang) converting enzyme-2 (ACE2) was discovered two decades ago as an RAS component, exhibiting a counter-regulatory role and opposing the adverse cardiovascular effects produced by Ang-II. Studies using synthetic compounds that can sustain the elevation of ACE2 activity or genetically overexpressed ACE2 in specific brain regions found various beneficial effects on cardiovascular function. More recently, ACE2 has been shown to play critical roles in neuro-inflammation, gut dysbiosis and the regulation of stress and anxiety-like behaviors. In the present review, we aim to highlight the anatomical locations and functional implication of brain ACE2 related to its BP regulation via modulation of the sympathetic nervous system and discuss the recent developments and future directions in the ACE2-mediated central cardiovascular regulation.