Current Hypertension Reports

, Volume 7, Issue 1, pp 61–67

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

Authors

  • Ivonne H. Schulman
    • Nephrology-Hypertension SectionUniversity of Miami School of Medicine, Veterans Affairs Medical Center
  • Ming-Sheng Zhou
    • Nephrology-Hypertension SectionUniversity of Miami School of Medicine, Veterans Affairs Medical Center
  • Leopoldo Raij
    • Nephrology-Hypertension SectionUniversity of Miami School of Medicine, Veterans Affairs Medical Center
Article

DOI: 10.1007/s11906-005-0056-6

Cite this article as:
Schulman, I.H., Zhou, M. & Raij, L. Current Science Inc (2005) 7: 61. doi:10.1007/s11906-005-0056-6

Abstract

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.

Copyright information

© Current Science Inc. 2005