© 1996 American Heart Association, Inc.
Articles |
Differential Regulation of L-Arginine Transport and Nitric Oxide Production by Vascular Smooth Muscle and Endothelium
From the Houston VA Medical Center and the Departments of Medicine (W.D., L.L., I.I., A.I.S.), Pharmacology (W.D.), and Molecular and Human Genetics (W.E.O.), Baylor College of Medicine, Houston, Tex.
Correspondence to Dr William Durante, Houston VA Medical Center, Bldg 109, Room 116, 2002 Holcombe Blvd, Houston, TX 77030.
Abstract Since NO production is dependent on the
availability of L-arginine, we examined whether
L-arginine transport and NO synthesis are coregulated by
vascular smooth muscle cells and endothelial cells
cultured from the same vessel wall source. L-Arginine
transport by both bovine aortic smooth muscle cells (BASMCs) and
endothelial cells (BAECs) was primarily Na+
independent (
70%) and was mediated by both a high- and
low-affinity transport system. Treatment of BASMCs with tumor
necrosis factor-
(TNF-) or interleukin-1ß (IL-1ß) resulted in
a significant increase in L-arginine transport (20%)
and in the induction of NO release. Exposure of BASMCs to interferon
gamma (IFN-
) or lipopolysaccharide (LPS) also stimulated
NO release but did not affect L-arginine transport. In
contrast, incubation of BAECs with TNF- or LPS strikingly enhanced
L-arginine uptake (2.5-fold), whereas IL-1ß and IFN-
had no effect. Treatment of BAECs with any of the inflammatory
mediators did not stimulate NO production. These results
demonstrate that L-arginine uptake and NO synthesis by
these cells are differentially regulated. In BASMCs, the coinduction of
L-arginine transport and NO formation may function to
provide increased levels of substrate to the cell during activation of
the NO synthase enzyme. In contrast, the selective stimulation of
L-arginine uptake in BAECs indicates that
L-arginine transport is dissociated from NO generation in
these cells.
Key Words: nitric oxide synthase • amino acids • smooth muscle • endothelium
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