AJP - Lung Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol 274: L360-L368, 1998;
1040-0605/98 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Miles, P. R.
Right arrow Articles by Huffman, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Miles, P. R.
Right arrow Articles by Huffman, L.
Vol. 274, Issue 3, L360-L368, March 1998

Constitutive nitric oxide production by rat alveolar macrophages

P. R. Miles1,2, L. Bowman1, A. Rengasamy1, and L. Huffman1,2

1 Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown 26505; and 2 Department of Physiology, West Virginia University School of Medicine, Morgantown, West Virginia 26506

Results from previous studies suggest that alveolar macrophages must be exposed to inflammatory stimuli to produce nitric oxide (· NO). In this study, we report that naive unstimulated rat alveolar macrophages do produce · NO and attempt to characterize this process. Western blot analysis demonstrates that the enzyme responsible is an endothelial nitric oxide synthase (eNOS). No brain or inducible NOS can be detected. The rate of · NO production is ~0.07 nmol · 106 cells-1 · h-1, an amount that is less than that produced by the eNOS found in alveolar type II or endothelial cells. Alveolar macrophage · NO formation is increased in the presence of extracellular L-arginine, incubation medium containing magnesium and no calcium, a calcium ionophore (A-23187), or methacholine. · NO production is inhibited by NG-nitro-L-arginine methyl ester (L-NAME) but not by NG-nitro-L-arginine, L-N5-(1-iminomethyl)ornithine hydrochloride, or aminoguanidine. Incubation with ATP, ADP, or histamine also inhibits · NO formation. Some of these properties are similar to and some are different from properties of eNOS in other cell types. Cellular · NO levels do not appear to be related to ATP or lactate content. Alveolar macrophage production of · NO can be increased approximately threefold in the presence of lung surfactant or its major component, dipalmitoyl phosphatidylcholine (DPPC). The DPPC-induced increase in · NO formation is time and concentration dependent, can be completely inhibited by L-NAME, and does not appear to be related to the degradation of DPPC by alveolar macrophages. These results demonstrate that unstimulated alveolar macrophages produce · NO via an eNOS and that lung surfactant increases · NO formation. This latter effect may be important in maintaining an anti-inflammatory state in vivo.

lung surfactant; dipalmitoyl phosphatidylcholine; nitric oxide synthase


This article has been cited by other articles:


Home page
 Cancer Res.Home page
L. R. Kisley, B. S. Barrett, A. K. Bauer, L. D. Dwyer-Nield, B. Barthel, A. M. Meyer, D. C. Thompson, and A. M. Malkinson
Genetic Ablation of Inducible Nitric Oxide Synthase Decreases Mouse Lung Tumorigenesis
Cancer Res., December 1, 2002; 62(23): 6850 - 6856.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
S. A. McDowell, A. Mallakin, C. J. Bachurski, K. Toney-Earley, D. R. Prows, T. Bruno, K. H. Kaestner, D. P. Witte, H. Melin-Aldana, S. J. F. Degen, et al.
The Role of the Receptor Tyrosine Kinase Ron in Nickel-Induced Acute Lung Injury
Am. J. Respir. Cell Mol. Biol., January 1, 2002; 26(1): 99 - 104.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
S.-H. Su, H.-i. Chen, and C. J. Jen
C57BL/6 and BALB/c Bronchoalveolar Macrophages Respond Differently to Exercise
J. Immunol., November 1, 2001; 167(9): 5084 - 5091.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
L. Connelly, M. Palacios-Callender, C. Ameixa, S. Moncada, and A. J. Hobbs
Biphasic Regulation of NF-{{kappa}}B Activity Underlies the Pro- and Anti-Inflammatory Actions of Nitric Oxide
J. Immunol., March 15, 2001; 166(6): 3873 - 3881.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
G. Ménard and E. Y. Bissonnette
Priming of Alveolar Macrophages by Leukotriene D4 . Potentiation of Inflammation
Am. J. Respir. Cell Mol. Biol., October 1, 2000; 23(4): 572 - 577.
[Abstract] [Full Text]

Home page
 PediatricsHome page
O. Aikio, K. Vuopala, M.-L. Pokela, and M. Hallman
Diminished Inducible Nitric Oxide Synthase Expression in Fulminant Early-Onset Neonatal Pneumonia
Pediatrics, May 1, 2000; 105(5): 1013 - 1019.
[Abstract] [Full Text]

Home page
 J. Immunol.Home page
J. Sirois, G. Menard, A. S. Moses, and E. Y. Bissonnette
Importance of Histamine in the Cytokine Network in the Lung Through H2 and H3 Receptors: Stimulation of IL-10 Production
J. Immunol., March 15, 2000; 164(6): 2964 - 2970.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
A. Nishiyama-Naruke and R. Curi
Phosphatidylcholine participates in the interaction between macrophages and lymphocytes
Am J Physiol Cell Physiol, March 1, 2000; 278(3): C554 - C560.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
K. R. WALLEY, T. E. MCDONALD, Y. HIGASHIMOTO, and S. HAYASHI
Modulation of Proinflammatory Cytokines by Nitric Oxide in Murine Acute Lung Injury
Am. J. Respir. Crit. Care Med., August 1, 1999; 160(2): 698 - 704.
[Abstract] [Full Text]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
P. R. Miles, L. Bowman, K. M. K. Rao, J. E. Baatz, and L. Huffman
Pulmonary surfactant inhibits LPS-induced nitric oxide production by alveolar macrophages
Am J Physiol Lung Cell Mol Physiol, January 1, 1999; 276(1): L186 - L196.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online