Acute and chronic hypoxic pulmonary vasoconstriction: a central role for endothelin-1?
In the pulmonary circulation, a decrease in oxygen tension results in the development of hypoxic pulmonary vasoconstriction (HPV), although the exact mechanism by which HPV occurs remains unclear. Evidence gathered from many laboratories suggests that while pulmonary arterial smooth muscle cells (PASMCs) can sense and respond to changes in oxygen tension, full expression of HPV requires modulating influences from the endothelium. In this review, we propose a model of HPV, based on recent studies from our laboratory, in which endothelin-1 (ET-1), a vasoactive peptide released from the endothelium, plays a central role and discuss how this model may be involved in the long-term adaptation to hypoxia.
Shimoda
Larissa A
LA
Division of Pulmonary and Critical Care Medicine, The Johns Hopkins University School of Medicine, 5501 Hopkins Bayview Circle, JHAAC 4A.52, Baltimore, MD 21224, USA. shimodal@welch.jhu.edu
Sham
James S K
JS
Liu
Qiang
Q
Sylvester
J T
JT
D000208:Acute Disease; D000818:Animals; D002908:Chronic Disease; D019332:Endothelin-1 / Q000502:physiology*; D000860:Hypoxia / Q000503:physiopathology*; D011652:Pulmonary Circulation / Q000502:physiology*; D014661:Vasoconstriction / Q000502:physiology*
D019332:Endothelin-1