Oxygen-sensing potassium currents in pulmonary artery

The pulmonary vasculature is sensitive to the relative components of the respiratory gases and will vasoconstrict in response to decreased oxygen (O2) levels. This hypoxic pulmonary vasoconstriction (HPV) controls pulmonary blood flow in the fetus and serves to maximize ventilation perfusion matching in the adult lung. The exact mechanism of HPV is not fully understood but it appears to involve direct effects on both the endothelium and smooth muscle cells within the vessel wall. There is growing evidence to suggest that hypoxia mediates vasoconstriction, at least in part through the inhibition of outward potassium (K+) current in smooth muscle. A number of K+ currents present in the pulmonary vasculature have been shown to be sensitive to O2, with hypoxia acting to inhibit these currents in the majority of cases. Differences in the expression of these O2-sensitive K+ channels may explain regional and generic variations observed in the HPV response. The mechanism by which these K+ channels sense changes in O2 levels may involve changes in the cellular redox state, oxidative phosphorylation or a direct effect on the channel protein itself.