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Hypoxic pulmonary vasoconstriction matches perfusion to ventilation and optimizes systemic oxygenation. Alterations in PO(2) are sensed by a vascular redox O(2) sensor in the pulmonary artery smooth muscle cell, probably within the mitochondria. This creates a signal that modulates redox-sensitive K(+) channels, thereby controlling membrane potential, Ca(2+) entry, and tone.
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Archer et al. (2002) studied this question.
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