High Blood Pressure

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-Angiotensin–Aldosterone System (RAAS). This system consists mainly of a 2-step enzymatic cascade catalyzed by renin and Angiotensin-Converting Enzyme (ACE), generating Ang II [1], 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.

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Last date updated on April, 2024