Understanding the central angiotensinergic and oxidative stress pathways in neurogenic hypertension may provide a foundation for future centrally-acting antioxidant therapies.
Cautions against clinical use of central antioxidants; leaves open whether SFO-PVN-RVLM targeting improves neurogenic hypertension outcomes.
Neurogenic hypertension has been the subject of extensive research worldwide. This review is based on the premise that some forms of neurogenic hypertension are caused in part by the formation of angiotensin-II (Ang-II)-induced reactive oxygen species along the subfornical organ-paraventricular nucleus of the hypothalamus-rostral ventrolateral medulla pathway (SFO-PVN-RVLM pathway). We will discuss the recent contribution of our laboratory and others regarding the mechanisms by which neurons in the SFO (an important circumventricular organ) are activated by Ang-II, how the SFO communicates with two other important areas involved in sympathetic activity regulation (PVN and RVLM) and how Ang-II-induced reactive oxygen species participate along the SFO-PVN-RVLM pathway in the pathogenesis of neurogenic hypertension.
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Braga et al. (2011) studied this question.
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