One explanation of the mechanism of hypoxic pulmonary vasoconstriction (HPV) suggests that hypoxia shifts the redox status of the pulmonary artery smooth muscle cell towards a more reduced state, through changes in the redox couples and the activated oxygen species generation. The outward K+ current is then reduced and the membrane depolarized, leading to Ca+2 influx through the voltage dependent Ca+2 channels and vasoconstriction. The response of both pulmonary and systemic vessels to hypoxia may depend on the expression of different K+ channels in the two sites. While the oxygen sensor in pulmonary artery smooth muscle cells may be the delayed rectifier K+ channel, in the systemic arteries, hyperpolarization of the smooth muscle cell membrane, leading to vasodilatation, probably represents the effect of hypoxia in opening ATP-sensitive and Ca+2-dependent K+ channels. The similarities between oxygen sensing mechanisms in several oxygen sensing cells (pulmonary artery smooth muscle cell, carotid body type 1 cell, neuroepithelial body) are striking. It is very likely that the mechanisms by which hypoxia is sensed at the molecular level are highly conserved and tightly regulated.