Document Detail

Cellular disposition of transported polyamines in hypoxic rat lung and pulmonary arteries.
MedLine Citation:
PMID:  10710534     Owner:  NLM     Status:  MEDLINE    
The polyamines putrescine, spermidine (SPD), and spermine are a family of low-molecular-weight organic cations essential for cell growth and differentiation and other aspects of signal transduction. Hypoxic pulmonary vascular remodeling is accompanied by depressed lung polyamine synthesis and markedly augmented polyamine uptake. Cell types in which hypoxia induces polyamine transport in intact lung have not been delineated. Accordingly, rat lung and rat main pulmonary arterial explants were incubated with [(14)C]SPD in either normoxic (21% O(2)) or hypoxic (2% O(2)) environments for 24 h. Autoradiographic evaluation confirmed previous studies showing that, in normoxia, alveolar epithelial cells are dominant sites of polyamine uptake. In contrast, hypoxia was accompanied by prominent localization of [(14)C]SPD in conduit, muscularized, and partially muscularized pulmonary arteries, which was not evident in normoxic lung tissue. Hypoxic main pulmonary arterial explants also exhibited substantial increases in [(14)C]SPD uptake relative to control explants, and autoradiography revealed that enhanced uptake was most evident in the medial layer. Main pulmonary arterial explants denuded of endothelium failed to increase polyamine transport in hypoxia. Conversely, medium conditioned by endothelial cells cultured in hypoxic, but not in normoxic, environments enabled hypoxic transport induction in denuded arterial explants. These findings in arterial explants were recapitulated in rat cultured main pulmonary artery cells, including the enhancing effect of a soluble endothelium-derived factor(s) on hypoxic induction of [(14)C]SPD uptake in smooth muscle cells. Viewed collectively, these results show in intact lung tissue that hypoxia enhances polyamine transport in pulmonary artery smooth muscle by a mechanism requiring elaboration of an unknown factor(s) from endothelial cells.
P Babal; S M Manuel; J W Olson; M N Gillespie
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
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 Mar 
Date Detail:
Created Date:  2000-05-24     Completed Date:  2000-05-24     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  L610-7     Citation Subset:  IM    
Departments of Pharmacology and Pathology, University of South Alabama College of Medicine, Mobile, Alabama 36688, USA.
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MeSH Terms
Anoxia / metabolism*,  pathology
Biological Transport / drug effects
Culture Media / pharmacology
Lung / metabolism*,  pathology
Muscle, Smooth, Vascular / metabolism,  pathology
Polyamines / pharmacokinetics*
Pulmonary Artery / metabolism*,  pathology
Rats, Sprague-Dawley
Reference Values
Spermidine / pharmacokinetics*
Tissue Distribution
Grant Support
Reg. No./Substance:
0/Culture Media; 0/Polyamines; 124-20-9/Spermidine

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