The pulmonary vasculature is sensitive to the relative components of the re
spiratory gases and will vasoconstrict in response to decreased oxygen (O-2
) levels. This hypoxic pulmonary vasoconstriction (HPV) controls pulmonary
blood flow in the fetus and serves to maximize ventilation perfusion matchi
ng in the adult lung. The exact mechanism of HPV is not fully understood bu
t it appears to involve direct effects on both the endothelium and smooth m
uscle cells within the vessel wall. There is growing evidence to suggest th
at hypoxia mediates vasoconstriction, at least in part through the inhibiti
on of outward potassium (K+) current in smooth muscle. A number of K+ curre
nts present in the pulmonary vasculature have been shown to be sensitive to
O-2, with hypoxia acting to inhibit these currents in the majority of case
s. Differences in the expression of these O-2-sensitive K+ channels may exp
lain regional and generic variations observed in the HPV response. The mech
anism by which these K+ channels sense changes in O-2 levels may involve ch
anges in the cellular redox state, oxidative phosphorylation or a direct ef
fect on the channel protein itself. (C) 1999 Elsevier Science Inc. All righ
ts reserved.