Abstract
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.
Highlights
The mechanisms underlying neurogenic hypertension have been the subject of extensive research worldwide
This review is based on the premise that neurogenic hypertension is caused in part by the formation of angiotensin-II (Ang-II)-induced reactive oxygen species (ROS) along the subfornical organ-paraventricular nucleus of the hypothalamus-rostral ventrolateral medulla pathway (SFOPVN-RVLM pathway)
The most accepted hypothesis is that Ang-II, as any other circulating lipophobic substance, acts on neurons in specialized regions of the brain known as the circumventricular organs (CVOs), which lack the normal blood brain barrier, in order to alter the function of other brain regions protected by this important barrier that “filters” what enters the central nervous system
Summary
Angiotensin-II-induced reactive oxygen species along the SFO-PVN-RVLM pathway: implications in neurogenic hypertension. Laboratório de Tecnologia Farmacêutica, Universidade Federal da Paraíba, João Pessoa, PB, Brasil
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