Key result
Angiotensin-II-derived reactive oxygen species in the brain, particularly along the SFO-PVN-RVLM pathway, play a critical role in the pathogenesis of neurogenic hypertension.
This review highlights the mechanistic role of brain Angiotensin-II-derived reactive oxygen species in the development of neurogenic hypertension.
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Brain ROS pathway warrants targeted investigation in neurogenic hypertension; leaves open clinical translation of pathway-specific therapies.
Hypertension and its relation to free radicals have been matter of continuous research worldwide. This review is based on the premise that some forms of neurogenic hypertension is, in part, caused by the formation of Angiotensin- II (Ang II)-derived reactive oxygen species within the brain, especially in areas along the Subfornical Organ- Paraventricular Nucleus of the Hypothalamus-Rostral Ventrolateral Medulla pathway (SFO-PVN-RVLM pathway). Here we will discuss the recent contribution of our laboratory and others regarding the mechanisms by which neurons in the Rostral Ventrolateral Medulla (RVLM) are activated by Ang II, how they communicate with the SFO and PVN and more importantly, how Ang II-derived Reactive Oxygen Species (ROS) participate along the SFO-PVN-RVLM pathway in the pathogenesis of neurogenic hypertension.
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Alynne S Carvalho (2012) conducted a review in Neurogenic hypertension. Angiotensin-II-derived reactive oxygen species was evaluated. Angiotensin-II-derived reactive oxygen species in the brain, particularly along the SFO-PVN-RVLM pathway, play a critical role in the pathogenesis of neurogenic hypertension.
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