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Developmental Regulation of Oxygen Sensing and Ion Channels in the Pulmonary Vasculature

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Membrane Receptors, Channels and Transporters in Pulmonary Circulation

Part of the book series: Advances in Experimental Medicine and Biology ((volume 661))

Abstract

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-1α (HIF-1α), 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.

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Correspondence to David N. Cornfield .

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Cornfield, D.N. (2010). Developmental Regulation of Oxygen Sensing and Ion Channels in the Pulmonary Vasculature. In: Yuan, JJ., Ward, J. (eds) Membrane Receptors, Channels and Transporters in Pulmonary Circulation. Advances in Experimental Medicine and Biology, vol 661. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-60761-500-2_13

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