Nitric oxide, oxidative stress and inflammation in pulmonary arterial hypertension
Posted Nov 18 2010 1:55am
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.
Some people with existing conditions may be at an increased risk of developing PAH, such as those with
Connective tissue diseases Systemic sclerosis (scleroderma)
Systemic lupus erythematosus, mixed connective tissue disease, rheumatoid arthritis and other connective tissue diseases
Congenital Heart Disease
Patients with a familial history of primary pulmonary hypertension
In addition to other diseases, exposure to specific toxins can also cause PAH. These include
Use of appetite-suppressant drugs such as fenfluramine or dexfenfluramine
Use of cocaine, methamphetamine or other street drugs
Exposure to toxins in contaminated food or the environment