Send to

Choose Destination
See comment in PubMed Commons below
Curr Hypertens Rep. 2005 Feb;7(1):61-7.

Nitric oxide, angiotensin II, and reactive oxygen species in hypertension and atherogenesis.

Author information

Nephrology-Hypertension Section, University of Miami School of Medicine, Veterans Affairs Medical Center, 1201 NW 16 Street (Room A-1009), Miami, FL 33125, USA.


A balance among nitric oxide (NO), angiotensin II (Ang II), and reactive oxygen species (ROS) in the endothelium is necessary for maintaining the homeostasis of the vascular wall. Oxidative stress has been shown to play a critical role in the development of hypertension and atherosclerosis. Although there is overwhelming evidence that hypertension promotes atherosclerosis, the relative contribution and/or interaction of hemodynamic and oxidative stress remains undefined. NO is synthesized in the endothelium by NO synthase and antagonizes the vasoconstrictive and proatherosclerotic effects of Ang II. On the other hand, Ang II decreases NO bioavailability by promoting oxidative stress. A better understanding of the pathophysiologic mechanisms involved in the link between hypertension and atherosclerosis may aid in developing therapeutic interventions. We propose that those antihypertensive agents that lower blood pressure and concomitantly restore the homeostatic balance of vasoactive agents in the endothelium would be more effective in preventing or arresting atherosclerosis.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Loading ...
    Support Center