ABSTRACT Background: High altitude pulmonary edema, HAPE, is a form of non-cardiogenic, non-inflammatory hydrostatic pulmonary edema that develops within the first days after rapid ascent to altitudes above 2500 to 3000 meters. Some individuals are shown to be more susceptible to the development of HAPE than others, these individuals have an increased pulmonary vasoconstriction in response to hypoxia compared to individuals shown to be resistant to HAPE. Objective: Performing a relevant search of current literature discussing the role of nitric oxide in the pathogenesis of high altitude pulmonary edema.Method: A methodical search of primary sources using PUBMED Medline, by performing a limited search using the search term: ( (High altitude pulmonary edema) AND (nitric oxide) NOT gene) Limits: English, Humans. 21 articles was identified, of these six articles was included in this literature review.Results: Inhalation of nitric oxide decreases pulmonary artery pressure in HAPE susceptible individuals exposed to hypoxia. HAPE susceptible individuals have decreased pulmonary exhaled nitric oxide in response to hypoxia, they also have decreased nitrate-nitrite levels in serum and their BAL fluid when exposed to hypoxia. Conclusion: Decreased production of nitric oxide by the lung endothelium can be a contributing factor or a direct cause to the increased pulmonary vasoconstriction seen in individuals prone to HAPE. However an increase in pulmonary vascular tone is only one mechanism contributing to the complex pathogenesis of high-altitude pulmonary edema. The nature of other underlying mechanisms is yet to be unravelled.