There is a well established relationship between the obstructive sleep apnea syndrome and hypertension. Current evidence suggests that the increase in arterial pressure is secondary to an enhanced sympathetic tone through peripheral chemoreflexes triggered by intermittent hypoxic stimulation of the carotid bodies. Chronic intermittent hypoxia would activate renal and systemic vasoactive systems through potentiated hypoxic chemoreflexes. These early changes in autonomic tone can be detected through cardiovascular variability and baroreflex sensitivity analysis. Both are relatively simple and noninvasive techniques. The multiplicity of pathogenic mechanisms in obstructive sleep apnea-associated hypertension emphasizes the need of increasing diagnostic sensitivity to detect and correct this common condition, which significantly increases cardiovascular risk.