Nitric oxide, oxidative stress and inflammation in pulmonary arterial hypertension

J Hypertens. 2010 Feb;28(2):201-12. doi: 10.1097/HJH.0b013e328332bcdb.


Pulmonary arterial hypertension (PAH) is a chronic and progressive disease characterized by a persistent elevation of pulmonary artery pressure accompanied by right ventricular hypertrophy (RVH). The current treatment for pulmonary hypertension is limited and only provides symptomatic relief due to unknown cause and pathogenesis of the disease. Both vasoconstriction and structural remodeling (enhanced proliferation of vascular smooth muscle cell) of the pulmonary arteries contribute to the progressive course of PAH, irrespective of different underlying causes. The exact molecular mechanism of PAH, however, is not fully understood. The purpose of this review is to provide recent advances in the mechanistic investigation of PAH. Specifically, this review focuses on nitric oxide, oxidative stress and inflammation and how these factors contribute to the development and progression of PAH. This review also discusses recent and potential therapeutic advancements for the treatment of PAH.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Chemokines / physiology
  • Cytokines / physiology
  • Endothelin Receptor Antagonists
  • Humans
  • Hypertension, Pulmonary / drug therapy
  • Hypertension, Pulmonary / etiology*
  • Hypertension, Pulmonary / physiopathology*
  • Inflammation / physiopathology
  • Isoprostanes / therapeutic use
  • Models, Biological
  • Nitric Oxide / physiology*
  • Nitric Oxide / therapeutic use
  • Oxidative Stress
  • Phosphodiesterase Inhibitors / therapeutic use
  • Pulmonary Artery / pathology
  • Pulmonary Artery / physiopathology
  • Reactive Oxygen Species / metabolism


  • Chemokines
  • Cytokines
  • Endothelin Receptor Antagonists
  • Isoprostanes
  • Phosphodiesterase Inhibitors
  • Reactive Oxygen Species
  • Nitric Oxide