Role of nitric oxide in the pathogenesis of chronic pulmonary hypertension
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
- MeSH
- Endothelium, Vascular drug effects metabolism MeSH
- Vascular Resistance drug effects physiology MeSH
- Chronic Disease MeSH
- Adult MeSH
- Enzyme Inhibitors pharmacology MeSH
- Humans MeSH
- Infant, Newborn MeSH
- Nitric Oxide metabolism pharmacology MeSH
- Lung blood supply drug effects embryology MeSH
- Hypertension, Pulmonary etiology metabolism MeSH
- Pulmonary Circulation drug effects physiology MeSH
- Nitric Oxide Synthase Type II MeSH
- Nitric Oxide Synthase Type III MeSH
- Nitric Oxide Synthase antagonists & inhibitors metabolism MeSH
- Vasodilation drug effects physiology MeSH
- Vasoconstriction drug effects physiology MeSH
- Free Radicals metabolism pharmacology MeSH
- Animals MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Infant, Newborn MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Enzyme Inhibitors MeSH
- NOS2 protein, human MeSH Browser
- NOS3 protein, human MeSH Browser
- Nitric Oxide MeSH
- Nitric Oxide Synthase Type II MeSH
- Nitric Oxide Synthase Type III MeSH
- Nitric Oxide Synthase MeSH
- Free Radicals MeSH
Chronic pulmonary hypertension is a serious complication of a number of chronic lung and heart diseases. In addition to vasoconstriction, its pathogenesis includes injury to the peripheral pulmonary arteries leading to their structural remodeling. Increased pulmonary vascular synthesis of an endogenous vasodilator, nitric oxide (NO), opposes excessive increases of intravascular pressure during acute pulmonary vasoconstriction and chronic pulmonary hypertension, although evidence for reduced NO activity in pulmonary hypertension has also been presented. NO can modulate the degree of vascular injury and subsequent fibroproduction, which both underlie the development of chronic pulmonary hypertension. On one hand, NO can interrupt vascular wall injury by oxygen radicals produced in increased amounts in pulmonary hypertension. NO can also inhibit pulmonary vascular smooth muscle and fibroblast proliferative response to the injury. On the other hand, NO may combine with oxygen radicals to yield peroxynitrite and other related, highly reactive compounds. The oxidants formed in this manner may exert cytotoxic and collagenolytic effects and, therefore, promote the process of reparative vascular remodeling. The balance between the protective and adverse effects of NO is determined by the relative amounts of NO and reactive oxygen species. We speculate that this balance may be shifted toward more severe injury especially during exacerbations of chronic diseases associated with pulmonary hypertension. Targeting these adverse effects of NO-derived radicals on vascular structure represents a potential novel therapeutic approach to pulmonary hypertension in chronic lung diseases.
References provided by Crossref.org
BDNF secretion by human pulmonary artery endothelial cells in response to hypoxia
