The mechanism(s) of hypoxic pulmonary vasoconstriction: potassium channels, redox O(2) sensors, and controversies

Abstract

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.