Specifically, the upregulation of the expression of angiotensinogen, ACE and AT1 receptors could play a significant role in the augmented carotid chemoreceptor activity, via the increased activity of chemoreflex, contributing to the pathophysiology of sleep apnea and the sympatho-excitation that is central to the endothelial dysfunction and heart failure during the course of pathogenesis. This evidence concerns the gene ACE and sleep apnea syndrome.