Reactive Oxygen Species, NADPH Oxidases, and Hypertension

被引:119
作者
Datla, Srinivasa Raju [1 ]
Griendling, Kathy K. [1 ]
机构
[1] Emory Univ, Div Cardiol, Dept Med, Sch Med, Atlanta, GA 30322 USA
基金
美国国家卫生研究院;
关键词
EXTRACELLULAR-SUPEROXIDE DISMUTASE; II-INDUCED HYPERTENSION; SALT-SENSITIVE RATS; ANGIOTENSIN-II; OXIDATIVE STRESS; MINERALOCORTICOID RECEPTOR; NAD(P)H OXIDASE; NITRIC-OXIDE; CARDIAC-HYPERTROPHY; BLOOD-PRESSURE;
D O I
10.1161/HYPERTENSIONAHA.109.142422
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
One concept that emerges from the recent Hypertension articles reviewed here is the existence of ROS-induced feed-forward loops in the cardiovascular system. This notion adds more complexity to cardiovascular ROS signaling, but at the same time helps to improve our understanding of the multiple roles of ROS in cardiovascular pathology. There appear to be 3 different loops: (1) cross-activation of different receptors; (2) activation of 1 ROS source by another; and (3) cross-talk between organ systems. More specifically, a feedforward loop exists between Ang II and MR systems. Acti-vation of 1 system, Ang II for example, can lead to indirect activation of the other (eg, MR), and vice versa. Thus, specific receptor blockers of AT1R or MR prevent the subsequent activation of the MR or AT1R, respectively. With respect to ROS-induced ROS generation, a feed-forward loop occurs between Nox and mitochondria in both the neuronal and vascular systems. Last but not least, stimulation of ROS signals in one organ can trigger ROS generation in other organs, as when the central alteration of O2̇- levels induces vascular inflammation. © 2010 American Heart Association, Inc.
引用
收藏
页码:325 / 330
页数:6
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