Purpose of Review Although an independent brain renin-angiotensin system is often assumed to exist, evidence for this concept is weak. Most importantly, renin is lacking in the brain, and both brain angiotensinogen and angiotensin (Ang) II levels are exceptionally low. In fact, brain Ang II levels may well represent uptake of circulating Ang II via Ang II type 1 (AT1) receptors. Recent Findings Nevertheless, novel drugs are now aimed at the brain RAS, i.e., aminopeptidase A inhibitors should block Ang III formation from Ang II, and hence diminish AT1 receptor stimulation by Ang III, while AT2 and Mas receptor agonists are reported to induce neuroprotection after stroke. The endogenous agonists of these receptors and their origin remain unknown. Summary This review addresses the questions whether independent angiotensin generation truly occurs in the brain, what its relationship with the kidney is, and how centrally acting RAS blockers/agonists might work.

Additional Metadata
Keywords Brain renin-angiotensin system .AminopeptidaseAinhibitor .AT2 receptor .Angiotensinogen .Kidney .Sympathetic nervous system . Stroke
Persistent URL dx.doi.org/10.1007/s11906-019-0937-8, hdl.handle.net/1765/116066
Journal Current Hypertension Reports
Citation
Ren, L, Lu, X, & Danser, A.H.J. (2019). Revisiting the Brain Renin-Angiotensin SystemFocus on Novel Therapies. Current Hypertension Reports, 21(4). doi:10.1007/s11906-019-0937-8