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lüll Developmental programming of O(2) sensing by neonatal intermittent hypoxia via epigenetic mechanisms Nanduri J; Prabhakar NRRespir Physiol Neurobiol 2013[Jan]; 185 (1): 105-9Recurrent apnea with intermittent hypoxia (IH) is a major clinical problem in infants born preterm. Carotid body chemo-reflex and catecholamine secretion from adrenal medullary chromaffin cells (AMC) are important for maintenance of cardio-respiratory homeostasis during hypoxia. This article highlights studies on the effects of IH on O(2) sensing by the carotid body and AMC in neonatal rodents. Neonatal IH augments hypoxia-evoked carotid body sensory excitation and catecholamine secretion from AMC which are mediated by reactive oxygen species (ROS)-dependent recruitment of endothelin-1 and Ca(2+) signaling, respectively. The effects of neonatal IH persist into adulthood. Evidence is emerging that neonatal IH initiates epigenetic mechanisms involving DNA hypermethylation contributing to long-lasting increase in ROS levels. Since adult human subjects born preterm exhibit higher incidence of sleep-disordered breathing and hypertension, DNA hypomethylating agents might offer a novel therapeutic intervention to decrease long-term cardio-respiratory morbidity caused by neonatal IH.|*Epigenesis, Genetic[MESH]|Adrenal Medulla/physiology[MESH]|Animals[MESH]|Animals, Newborn[MESH]|Carotid Body/*physiology[MESH]|Chromaffin Cells/*physiology[MESH]|Fetal Hypoxia/*genetics[MESH]|Humans[MESH]|Infant, Newborn[MESH]|Infant, Premature[MESH]|Oxygen/*blood[MESH] |