Angiotensin-II-induced reactive oxygen species along the SFO-PVN-RVLM pathway: implications in neurogenic hypertension

V.A. Braga, I.A. Medeiros, T.P. Ribeiro, M.S. França-Silva, M.S. Botelho-Ono and D.D. Guimarães
Laboratório de Tecnologia Farmacêutica, Universidade Federal da Paraíba, João Pessoa, PB, Brasil.

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2011007500088&lng=en&nrm=iso&tlng=en

This is an interesting review about how angiotensin-II (Ang-II)-induced reactive oxygen species (ROS) produces some forms of neurogenic hypertension. The most interesting aspect is that it discusses about the three important areas, subfornical organ (SFO), paraventricular nucleus (PVN) and rostral ventrolateral medulla (RVLM) and their contributions individually and in combination with one another for the pathogensis of neurogenic hypertension. Direct microinjection studies in the brain using Ang-II have shown that oxidative stress is an important mechanism by which Ang-II increases blood pressure. However the question of how circulating Ang-II acts on these brain centers without crossing blood brain barrier, resulting in increased sympathetic nerve activity and causing hypertension remains to be answered. Numerous hypothesis have been postulated, one widely accepted hypothesis is that Ang-II acts on the neurons in the circumventricualr organ (CVO) which lacks blood brain barrier, which inturn alter the other brian regions by increasing the production of local Ang-II. This review mainly address the mechanisms by which Ang-II acts on the neurons in the SFO (one of the CVOs), and how SFO communicates with PVN and RVLM in ROS production, regulating sympathetic activation and altering blood pressure. This review points out at numerous studies that directly and indirectly have shown how ROS production in all the three regions SFO, PVN and RVLM could contribute to neurogenic hypertension. The figure in the last page summarizes how Ang-II could induce the production of ROS and inturn neuronal firing.  The possible pathway interconnecting all these regions to the pathogenesis of neurogenic hypertension could have been more elaborate.

- Madhan