Constitutive nitric oxide production by rat alveolar macrophages
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 expose...
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Published in | American journal of physiology. Lung cellular and molecular physiology Vol. 274; no. 3; pp. 360 - L368 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
01.03.1998
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Subjects | |
Online Access | Get full text |
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Summary: | 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 · 10 6
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
N G -nitro- L -arginine methyl ester
( L -NAME) but not by
N G -nitro- L -arginine,
L - N 5 -(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 |
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ISSN: | 1040-0605 0002-9513 1522-1504 |
DOI: | 10.1152/ajplung.1998.274.3.L360 |