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Mitochondrial Reactive Oxygen Species and Redox State in Pulmonary Vascular O2 Sensing

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Abstract

Mammals possess a homeostatic O2-sensing system that comprises the resistance pulmonary arteries, ductus arteriosus, carotid body, neuroepithelial body, systemic arteries, fetal adrenomedullary cell, and fetoplacental arteries. Together these specialized tissues form a homeostatic system that increases the organism’s ability to survive hypoxia, whether encountered during development, at altitude, or during disease. Thus, the homeostatic O2-sensing system optimizes O2 uptake and delivery. One important part of the homeostatic O2-sensing system is hypoxic pulmonary vasoconstriction (HPV), a vasomotor response of resistance pulmonary arteries to alveolar hypoxia, that optimizes ventilation/perfusion matching and optimizes systemic O2 tension. The core mechanisms of hypoxic pulmonary vasoconstriction resides in the smooth muscle cell, although it is modulated by the endothelium. This chapter explores and updates the redox theory for the mechanism of hypoxic pulmonary vasoconstriction.

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Archer, S.L., Ryan, J.J. (2011). Mitochondrial Reactive Oxygen Species and Redox State in Pulmonary Vascular O2 Sensing. In: Yuan, JJ., Garcia, J., West, J., Hales, C., Rich, S., Archer, S. (eds) Textbook of Pulmonary Vascular Disease. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-87429-6_19

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