Each of the potential mediating mechanisms in OSA may also be assessed in RLS, including 1) neural mechanisms such as increased central sympathetic outflow, impaired baroreflex function, diminished heart rate and blood pressure variability, and increased chemoreflex sensitivity, 2) metabolic mechanisms such as glucose intolerance and reduced insulin sensitivity/diabetes as a result of sleep disturbance in RLS, 3) oxidative stress, 4) systemic or vascular inflammatory mechanisms, and 5) vascular mechanisms including impaired endothelial functioning, increased aortic stiffness, hypothalamic-pituitary axis activation or renin-angiotensin-aldosterone activation.