title: Endothelial dysfunction in adults with obstructive sleep apnea.
abstract: Vascular endothelial dysfunction refers to a loss of normal homeostatic functions in the blood vessels. It is characterized by reduced vasodilation and enhanced vasoconstriction functions and chronic prothrombotic and inflammatory activity. There is convincing evidence for endothelial dysfunction in obstructive sleep apnea (OSA): OSA is associated with alterations in vascular structures and their elastic properties, increased circulating cell-derived microparticles, reduced endothelial repair capacity, and vascular reactivity. These alterations may be related to the reduced availability of nitric oxide, which has major vasoprotective effects including vasodilation, inhibition of platelet adhesion and aggregation, inhibition of leukocyte-endothelial adhesion and inhibition of smooth muscle cell proliferation. It is unknown whether endothelial dysfunction in OSA is due to alterations in vasoconstriction mechanisms related to angiotensin II or endothelin 1. In OSA, endothelial dysfunction may be related to chronic intermittent hypoxia and to sleep loss and fragmentation. These conditions may increase the levels of various markers of inflammation and oxidative stress, as well as those of increased procoagulant and thrombotic activity. In addition, they may produce an imbalance of vasomotor function. Endothelial dysfunction contributes to the development of atherosclerosis and cardiovascular disorders associated with OSA. However, other diseases that are also associated with endothelial dysfunction are OSA comorbidities, e.g. obesity, insulin resistance, smoking habits and cardiovascular diseases such as hypertension and coronary artery disease. This makes it difficult to demonstrate a causal link between OSA and endothelial dysfunction; nevertheless, evidence for such a link has been produced by therapeutic studies. The administration of continuous positive airway pressure may reverse changes associated with endothelial dysfunction and, therefore, may decrease the risk of cardiovascular disease in OSA patients.
mesh_terms: D000328:Adult; D000804:Angiotensin II / Q000378:metabolism; D017209:Apoptosis; D015415:Biomarkers / Q000378:metabolism; D001778:Blood Coagulation Disorders / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D045422:Continuous Positive Airway Pressure; D019332:Endothelin-1 / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress; D012307:Risk Factors; D020181:Sleep Apnea, Obstructive / Q000150:complications / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy*
chemical_list: D015415:Biomarkers; D019332:Endothelin-1; D000804:Angiotensin II; D009569:Nitric Oxide