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J. Biol. Chem., Vol. 275, Issue 51, 39807-39810, December 22, 2000
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From the Institute for Environmental Medicine, University of
Pennsylvania, Philadelphia, Pennsylvania 19104
Endothelial cells generate nitric oxide (NO) in
response to agonist stimulation or increased shear stress. In this
study, we evaluated the effects of abrupt cessation of shear stress on pulmonary endothelial NO generation and its relationship to changes in
intracellular Ca2+. In situ endothelial
generation of NO and changes in intracellular Ca2+ in
isolated, intact rat lungs were evaluated using fluorescence microscopy
with diaminofluorescein diacetate, an NO probe, and Fluo-3, a
Ca2+ probe. The onset of increased NO generation in
endothelial cells of subpleural microvessels in situ
occurred between 30 and 90 s after onset of ischemia and was
preceded by an increase in intracellular Ca2+ due to both
influx of extracellular Ca2+ and release from intracellular
stores. Flow cessation-induced NO generation in endothelial cells
in situ was Ca2+-, calmodulin-, and
PI3-kinase-dependent. The similarity of endothelial cell
response (increased NO generation) to either increased flow or
cessation of flow suggests that cells respond to an imposed alteration
from a state of adaptation. This response to flow cessation may
constitute a compensatory vasodilatatory mechanism and may play a role
in signaling for cell proliferation and vascular remodeling.
ACCELERATED PUBLICATION
Ca2+- and Phosphatidylinositol
3-Kinase-dependent Nitric Oxide Generation in Lung
Endothelial Cells in Situ with Ischemia*
, and
*
This work was supported by a Parker B. Francis fellowship
(to A. B. A.) and National Institutes of Health, Specialized
Center for Research in Acute Lung Injury Grant P50-HL60290 (to
A. B. F.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Present address: 2nd Department of Surgery, Akita University
School of Medicine, Akita, Japan.
§
To whom correspondence should be addressed: Institute for
Environmental Medicine, University of Pennsylvania Medical Center, One
John Morgan Bldg., 3620 Hamilton Walk, Philadelphia, PA 19104-6068. Tel.: 215-898-9100; Fax: 215-898-0868; E-mail: abf@mail.
med.upenn.edu.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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