Obstructive sleep apnea syndrome (OSAS) is a highly prevalent disease characterized by recurrent episodes of partial or complete obstruction of the upper airways during sleep, leading to oxygen desaturation, sleep fragmentation and clinical endothelial dysfunction. Microparticles (MPs) are membrane vesicles released during cell activation and apoptosis. Elevated levels of circulating MPs have been detected in pathologies associated with vascular alterations. We investigated the effects of MPs on endothelial function and vascular reactivity in OSAS. Blood samples were obtained either from 38 OSAS patients without any other cardiovascular comorbidities and 23 healthy subjects. A desaturation index above 10 per hour defined OSAS patients. MPs concentration and origin were assessed using flow cytometer. Male Swiss mice were injected i.v. with MPs from OSAS or healthy subjects, or with saline solution, and sacrified after 24hours. Endothelial function and vascular reactivity were studied on aortic rings and small mesenteric resistance (SMA) arteries by myography and arteriography, respectively. Patients with OSAS did not display increased circulating levels of MPs compared to healthy subjects including those from pro-coagulant, platelet, endothelial, leukocyte and erythrocyte origins. Interestingly, MPs from granulocytes and activated leukocytes were significantly enhanced in OSAS patients. Activated leukocyte MPs positively correlated with oxygen desaturation index. In aorta, MPs from OSAS patients but not those from healthy subjects significantly reduced endothelium-dependent relaxation to acetylcholine. MPs from OSAS increased sensitivity of the aorta in response to serotonin that was greater compared to the effect of MPs from healthy subjects. In SMA, MPs from OSAS but not those from healthy subjects impaired flow-induced dilation without any effect on myogenic tone. Although SMA from mice treated with healthy subjects MPs did not affect flow-induced dilation, these vessels showed a reduced prostacyclin-component that was completely compensated by the NO-component of the response. The endothelial dysfunction induced by MPs from OSAS was caused by the reduction of both NO- and prostacyclin- but not the endothelium-derived hyperpolarizing factor-components of the response in SMA. These data provide evidence that circulating MPs from OSAS patients influence both endothelial function and vascular reactivity.Le texte complet de cet article est disponible en PDF.