Department of Biotechnology, Biotechnology Center, Federal University of Paraiba João Pessoa, Brazil.
Front Physiol. 2013 May 13;4:105. doi: 10.3389/fphys.2013.00105. eCollection 2013.
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.
高血压是一种多因素疾病，与压力感受性反射敏感性（BRS）降低和自主神经功能障碍有关。多项研究表明，血管紧张素 II（Ang II）是肾素-血管紧张素-醛固酮系统（RAAS）的主要肽，通过激活 1 型受体（AT1R），可促使烟酰胺腺嘌呤二核苷酸磷酸（NAD(P)H）氧化酶产生过多的活性氧（ROS），这是 Ang II 引起高血压的核心机制。在本综述中，我们将讨论 Ang II 和氧化应激在高血压中的作用、BRS 与高血压发生之间的关系，以及氧化应激如何在几种高血压模型中引发压力感受性反射功能障碍。最后，我们将描述一些新型治疗药物，以在高血压期间改善 BRS。
