alexa Angiotensin-II Induced Reactive Oxygen Species: Implications in Neurogenic Hypertension | OMICS International | Abstract
ISSN: 2167-1095

Journal of Hypertension: Open Access
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Review Article

Angiotensin-II Induced Reactive Oxygen Species: Implications in Neurogenic Hypertension

LU Chengzhi1*, WANG Li2, Aubdool-Essackjee2, Nima Sherpa2 and LUO Di2

1Department of Cardiology, Tianjin First Central Hospital, Tianjin, China

2The Institute of Graduate, Tianjin Medical University, Tianjin, China

*Corresponding Author:
Dr. LU Cheng-zhi
Department of Cardiology
Tianjin First Central Hospital
Tianjin China,24, Fukang Road
Nankai District, Tianjin
300192, China
Tel: +86-022-23626585
Fax: +86-022-23626585
E-mail: [email protected]

Received Date: June 12, 2012; Accepted Date: July 17, 2012; Published Date: July 20, 2012

Citation: Chengzhi LU, Li W, Essackjee A, Sherpa N, Di LUO (2012) Angiotensin- II Induced Reactive Oxygen Species: Implications in Neurogenic Hypertension. J Hypertens 1:106. doi: 10.4172/2167-1095.1000106

Copyright: © 2012 Chengzhi LU, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Reactive oxygen species (ROS) play an important role in the development and maintenance cardio vascular
diseases, especially hypertension. The relationship between ROS and hypertension has been demonstrated in several models of experimental hypertension. Accumulating evidence has suggested that the key mechanism through which Angiotensin II (Ang II) influences blood pressure is via its ability to activate ROS signaling pathways. Ang II, by stimulating angiotensin AT1 receptors, involved in the activation of NAD(P)H oxidase, which is a major source of ROS production. Despite many elegant studies that have been accumulated regarding ROS/Ang II signaling, there is still much to be elucidated in the role of ROS in neurogenic hypertension. The present review mainly discussed some recent findings documenting about the signaling mechanisms of Ang II-induced ROS in neurogenic hypertension and therapeutic target.


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