In patients with obstructive sleep apnea (OSA), nocturnal exposure to intermittent hypoxia causes elevations in arterial pressure that persist throughout the day. Animal models have shown that this hypertensive effect requires an intact sympathetic nervous system and an intact carotid chemoreceptor reflex. The renin-angiotensin system contributes importantly to hypertension in this model, because renal nerve denervation, angiotensin II receptor blockade, and suppression of the renin-angiotensin system by high salt diet all prevent the rise in blood pressure. The vascular endothelium is functionally impaired in this model and also in patients with OSA. These individuals demonstrate decreased plasma levels of nitric oxide metabolites, increased production of superoxide by neutrophils, and increased levels of 8-isoprostane in breath condensate. Increased levels of pro-inflammatory cytokines are also present. Thus, oxidant stress and inflammation are potential mediators of intermittent hypoxia-induced vascular dysfunction. Once the mechanisms of intermittent hypoxia-induced alterations in vascular structure and function are understood, strategies can be developed to reverse or prevent them. Such research has relevance not only to hypertension, but also to atherosclerosis and other important cardiovascular sequelae of OSA.