Key result
The ACE-Ang II-AT1 and ACE2-Ang-(1-7)-Mas axes exert counter-regulatory effects on reactive oxygen species-mediated control of vascular tone and oxidative stress-elicited vascular dysfunction.
This review highlights the counter-regulatory roles of the ACE-Ang II-AT1 and ACE2-Ang-(1-7)-Mas axes in modulating reactive oxygen species and vascular function, providing a mechanistic basis for pharmacological interventions.
May inform dual RAS axis therapies in vascular disease; leaves open clinical translation via prospective trials.
The Renin-Angiotensin system plays an important role in the regulation of systemic blood pressure as well as in fluid and electrolyte balance. It is divided into two described axes, the ACE - Ang II - AT1 receptor, with Ang II as the main mediator, and the ACE2 - Ang-(1-7) - Mas receptor, with Ang-(1-7) responsible for the main effects. The main vascular effect induced by Ang II is contraction, while Ang-(1-7) includes relaxation in several vascular beds. Ang II also activates several cytokines that are important in the genesis of vascular inflammation and hypertrophy. In this context, Ang-(1-7) seems to have a protective role. Both AT1 and Mas receptors modulate, in different ways, the generation of, which are involved in the control of vascular tone and the genesis of vascular dysfunction triggered by several diseases, including diabetes mellitus, arterial hypertension and atherosclerosis. Thereby, this review presents an overview of the modulation played by the whole Renin-Angiotensin system on the reactive oxygen species-mediated control of vascular tone and the oxidative stress-elicited vascular dysfunction.
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Pernomian et al. (2014) conducted a review in Vascular dysfunction. Renin-Angiotensin system axes was evaluated. The ACE-Ang II-AT1 and ACE2-Ang-(1-7)-Mas axes exert counter-regulatory effects on reactive oxygen species-mediated control of vascular tone and oxidative stress-elicited vascular dysfunction.
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