Sleep disordered breathing manifested as recurrent apneas are the most frequently encountered respiratory disorders in adult humans and infants born preterm. Patients with recurrent apneas exhibit autonomic co-morbidities including hypertension, persistent sympathetic activation and elevated plasma catecholamines. Intermittent hypoxia (IH) resulting from apneas is the primary stimulus for evoking autonomic changes. Carotid bodies are the front-line defense during apneas and adrenal medullary chromaffin cells (AMC) are a major source of circulating catecholamines. In this presentation I review recent studies on the effects of IH on carotid body and AMC, their functional consequences, and the underlying cellular as well as molecular mechanisms. Studies on rodents demonstrate that IH sensitizes carotid body response to hypoxia and induces sensory long-term facilitation in response to repetitive hypoxia resulting in exaggerated chemo-reflex function that contributes to heightened sympathetic tone. IH markedly increases hypoxia-induced catecholamine secretion from AMC, which contributes to elevated plasma catecholamines. Reactive oxygen species (ROS) signaling is critical for mediating the effects of IH on carotid body and AMC. Cellular sources of ROS during include the activation of NADPH oxidases (Nox) and inhibition of mitochondrial complex I. In addition, IH up-regulates pro-oxidant and down-regulates anti-oxidant genes, and imbalance between transcriptional activators HIF-1 and HIF-2 contribute to this response.