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Endothelium-derived mediators and hypoxic pulmonary vasoconstriction
Philip I Aaronson1, Thomas P Robertson, Jeremy P T Ward
1Department of Respiratory Medicine and Allergy, Centre for Cardiovascular Biology and Medicine, Guy's, King's and St Thomas' School of Medicine, 5th Floor Thomas Guy House, King's College London, Guy's Campus, London SE1 9RT, UK.
Respiratory Physiology & Neurobiology
|July 20, 2002
Summary
The pulmonary vascular endothelium plays a role in hypoxic pulmonary vasoconstriction (HPV). An unidentified endothelium-derived agent may sensitize smooth muscle calcium, enabling sustained HPV.
Area of Science:
- Cardiovascular Physiology
- Pulmonary Circulation
- Endothelial Biology
Background:
- The vascular endothelium regulates pulmonary vascular resistance through vasoactive mediators.
- The endothelium's precise role in hypoxic pulmonary vasoconstriction (HPV) remains controversial.
- While HPV can occur without endothelium, sustained HPV often shows dependence on an intact endothelium.
Purpose of the Study:
- To review evidence for and against specific endothelium-derived mediators in HPV.
- To elucidate the facilitatory or permissive function of the endothelium in sustained HPV.
- To propose a mechanism involving an endothelium-derived agent in smooth muscle calcium sensitization.
Main Methods:
- Review of existing scientific literature on HPV and endothelial function.
- Analysis of studies investigating the role of endothelium-derived mediators.
- Synthesis of evidence to support a proposed mechanism of HPV.
Main Results:
- No single endothelium-derived mediator has been unequivocally proven essential for HPV.
- Evidence suggests the endothelium may facilitate or permit sustained HPV.
- Hypoxia may trigger the release of an unidentified agent from the endothelium.
Conclusions:
- The endothelium likely plays a facilitatory or permissive role in sustained HPV.
- This role involves interaction with smooth muscle intracellular calcium.
- An unidentified endothelium-derived agent may induce calcium sensitization in pulmonary artery smooth muscle during hypoxia.