Acute hypoxic pulmonary vasoconstriction: a model of oxygen sensing.

E. D. Michelakis, S. L. Archer, E. K. Weir

Research output: Contribution to journalReview articlepeer-review

23 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)361-367
Number of pages7
JournalPhysiological research / Academia Scientiarum Bohemoslovaca
Issue number6
StatePublished - 1995


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