Acute hypoxic pulmonary vasoconstriction: a model of oxygen sensing.
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.
Michelakis
E D
ED
Department of Medicine, Veterans Administration Medical Center, Minneapolis, USA.
Archer
S L
SL
Weir
E K
EK
D000818:Animals; D006801:Humans; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D010084:Oxidation-Reduction; D010100:Oxygen / Q000097:blood*; D011652:Pulmonary Circulation / Q000502:physiology*; D014661:Vasoconstriction / Q000502:physiology*
D010100:Oxygen