The mechanisms underlying neurogenic hypertension have been matter of continuous research worldwide. This review focus on the hypothesis that neurogenic hypertension is, in part, caused by the formation of Angiotensin-II (Ang II)-derived reactive oxygen species in key cardiovascular nuclei, especially in the Rostral Ventrolateral Medulla (RVLM). Ang II is the major effector of the Renin-AngiotensinâAldosterone System (RAAS). This system consists mainly of a 2-step enzymatic cascade catalyzed by renin and Angiotensin-Converting Enzyme (ACE), generating Ang II , the effect of Ang II is mediated by Ang II receptors. Two isoforms of Ang II receptor have been identified: type 1 receptor (AT1R) and type 2 receptor (AT2R). In general, it is accepted that cardiovascular effects of Ang II such as vasoconstriction, regulation of fluid and drinking behavior are ascribed to AT1R.
Carvalho AS, Brain Angiotensin-II-derived Reactive Oxygen Species: Implications for High Blood Pressure.
Last date updated on July, 2014