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Hypoxic pulmonary vasoconstriction: mechanisms and controversies
Philip I Aaronson1, Tom P Robertson, Gregory A Knock
1Department of Asthma, Allergy and Respiratory Science, New Hunt's House, Guy's Hospital Campus, King's College London, London SE1 1UL, UK. philip.aaronson@kcl.ac.uk
The Journal of Physiology
|October 29, 2005
Summary
Hypoxic pulmonary vasoconstriction (HPV) constricts pulmonary arteries during low oxygen, unlike systemic arteries. Mechanisms involve calcium signaling and rho kinase in pulmonary artery smooth muscle cells, though endothelium dependency remains unclear.
Area of Science:
- Cardiovascular Physiology
- Pulmonary Medicine
- Cellular Biology
Background:
- Pulmonary circulation uniquely constricts arteries during hypoxia (HPV), unlike systemic vasodilation.
- HPV maintains ventilation-perfusion matching in localized alveolar hypoxia.
- Global hypoxia in disease elevates pulmonary vascular resistance, stressing the right heart.
Purpose of the Study:
- To review recent findings and ongoing controversies in the mechanisms of HPV.
- To highlight the role of intracellular calcium and rho kinase in HPV.
- To discuss the endothelium's role in HPV.
Main Methods:
- Review of existing literature on HPV mechanisms.
- Analysis of studies investigating intracellular Ca2+ concentration ([Ca2+]i) in PASMC.
- Examination of evidence for rho kinase and endothelium dependency in HPV.
Main Results:
- Hypoxia stimulates pathways increasing [Ca2+]i in pulmonary artery smooth muscle cells (PASMC).
- HPV requires a small rise in [Ca2+]i and rho kinase-mediated Ca2+ sensitization.
- Endothelium dependency of HPV is supported by evidence but not fully explained.
Conclusions:
- Multiple pathways contribute to HPV, involving [Ca2+]i and Ca2+ sensitization.
- The precise mechanisms of HPV, including endothelium dependency, require further investigation.
- Understanding HPV is crucial for managing cardiovascular complications in hypoxic conditions.