Angiotensin-II-derived reactive oxygen species on baroreflex sensitivity during hypertension: new perspectives

Thyago M De Queiroz,Valdir A Braga,Matheus M O Monteiro

doi:10.3389/fphys.2013.00105

Abstract

Hypertension is a multifactorial disorder, which has been associated with the reduction in baroreflex sensitivity (BRS) and autonomic dysfunction. Several studies have revealed that increased reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate [NAD(P)H] oxidase, following activation of type 1 receptor (AT1R) by Angiotensin-(Ang) II, the main peptide of the Renin–Angiotensin–Aldosterone System (RAAS), is the central mechanism involved in Ang-II-derived hypertension. In the present review, we will discuss the role of Ang II and oxidative stress in hypertension, the relationship between the BRS and the genesis of hypertension and how the oxidative stress triggers baroreflex dysfunction in several models of hypertension. Finally, we will describe some novel therapeutic drugs for improving the BRS during hypertension.

Highlights

Hypertension is a multifactorial disorder, which has been associated with the reduction in baroreflex sensitivity (BRS) and autonomic dysfunction
Regarding Ang II effects on the central nervous system (CNS), a high density of Ang II type 1 receptors was found in specific regions of the forebrain and in the rostral ventrolateral medulla (RVLM) (Allen et al, 1998)
Using combined in vivo and molecular biology approaches, we have documented that Ang II-induced hypertension is mediated by an increase in sympathetic nerve activity, which seems to involve up-regulation of AT1 receptors in the RVLM and down-regulation of AT1 receptors in the subfornical organ (SFO) (Braga, 2011; Nunes and Braga, 2011)

Summary

Introduction

Hypertension is a multifactorial disorder, which has been associated with the reduction in baroreflex sensitivity (BRS) and autonomic dysfunction. Using combined in vivo and molecular biology approaches, we have documented that Ang II-induced hypertension is mediated by an increase in sympathetic nerve activity, which seems to involve up-regulation of AT1 receptors in the RVLM and down-regulation of AT1 receptors in the subfornical organ (SFO) (Braga, 2011; Nunes and Braga, 2011).

Results

Conclusion