| Aquaporin water channels and lung physiology. | |
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MedLine Citation:
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PMID: 10781416 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Fluid transport across epithelial and endothelial barriers occurs in the neonatal and adult lungs. Biophysical measurements in the intact lung and cell isolates have indicated that osmotic water permeability is exceptionally high across alveolar epithelia and endothelia and moderately high across airway epithelia. This review is focused on the role of membrane water-transporting proteins, the aquaporins (AQPs), in high lung water permeability and lung physiology. The lung expresses several AQPs: AQP1 in microvascular endothelia, AQP3 in large airways, AQP4 in large- and small-airway epithelia, and AQP5 in type I alveolar epithelial cells. Lung phenotype analysis of transgenic mice lacking each of these AQPs has been informative. Osmotically driven water permeability between the air space and capillary compartments is reduced approximately 10-fold by deletion of AQP1 or AQP5 and reduced even more by deletion of AQP1 and AQP4 or AQP1 and AQP5 together. AQP1 deletion greatly reduces osmotically driven water transport across alveolar capillaries but has only a minor effect on hydrostatic lung filtration, which primarily involves paracellular water movement. However, despite the major role of AQPs in lung osmotic water permeabilities, AQP deletion has little or no effect on physiologically important lung functions, such as alveolar fluid clearance in adult and neonatal lung, and edema accumulation after lung injury. Although AQPs play a major role in renal and central nervous system physiology, the data to date on AQP knockout mice do not support an important role of high lung water permeabilities or AQPs in lung physiology. However, there remain unresolved questions about possible non-water-transporting roles of AQPs and about the role of AQPs in airway physiology, pleural fluid dynamics, and edema after lung infection. |
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Authors:
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A S Verkman; M A Matthay; Y Song |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review |
Journal Detail:
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Title: American journal of physiology. Lung cellular and molecular physiology Volume: 278 ISSN: 1040-0605 ISO Abbreviation: Am. J. Physiol. Lung Cell Mol. Physiol. Publication Date: 2000 May |
Date Detail:
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Created Date: 2000-06-01 Completed Date: 2000-06-01 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 100901229 Medline TA: Am J Physiol Lung Cell Mol Physiol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: L867-79 Citation Subset: IM |
Affiliation:
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Departments of Medicine and Physiology, Cardiovascular Research Institute, University of California, San Francisco, California 94143-0521, USA. verkman@itsa.ucsf.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Aquaporins / metabolism* Humans Lung / physiology* Water / metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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HL42368/HL/NHLBI NIH HHS; HL51854/HL/NHLBI NIH HHS; HL60288/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Aquaporins; 7732-18-5/Water |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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