The increase in oxygen tension occurring at birth causes sustained and progressive pulmonary vasodilation. The oxygen-induced perinatal pulmonary vasodilation depends on the production of nitric oxide (NO) from the pulmonary endothelium and activation of various K+ channels in pulmonary artery smooth muscle cells. This chapter reviews a) the oxygen-sensing mechanism that stimulates endothelial NO production; b) how K+ channels sense changes in oxygen tension; c) whether hypoxia-inducible factor-1á (HIF-1á), a well defined hypoxia-sensitive transcription factor in adult, contributes to the regulation of NO production and K+ channel activation; and d) whether and how dysfunctional K+ channels contribute to the development of pulmonary hypertension in the newborns. © Humana Press, a part of Springer Science+ Business Media, LLC 2010.
CITATION STYLE
Cornfield, D. N. (2010). Developmental regulation of oxygen sensing and ion channels in the pulmonary vasculature. In Advances in Experimental Medicine and Biology (Vol. 661, pp. 201–220). https://doi.org/10.1007/978-1-60761-500-2_13
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