Sleep apnea is one of the most common respiratory disorders affecting adult humans and preterm infants globally. The disorder has been linked with several comorbidities including obesity and hypertension, and it is prevalent in patients with stroke, heart failure, and atrial arrhythmias. During sleep, recurring episodes of hypoxia, normoxia and hypercapnia act through diverse mechanisms to alter sympathetic drive in sleep apnea patients. The purpose of this review is to illustrate the neurophysiological mechanisms by which sleep apnea promotes the elevation of blood pressure and sympathetic activity, as well as to emphasize the increased cardiovascular risk present in patients with the disorder. Sleep apnea patients and rodent models of the disorder exhibit enhanced chemoreceptor sensitivity and reduced baroreceptor activity, both of which create a homeostatic imbalance that promotes blood pressure elevation. Studies in rodent models have also revealed that intermittent hypoxia augments the production of vasoactive hormones which contribute to enhanced blood pressure in sleep apnea. Thus, the interplay of sympathetic activation and vasoconstriction is able to trigger hypertension, which is a major risk factor for the development of several cardiovascular diseases including stroke and heart failure.