Circulation. 1998;97:108-112
(Circulation. 1998;97:108-112.)
© 1998 American Heart Association, Inc.
Atherosclerosis and the Two Faces of Endothelial Nitric Oxide Synthase
Robert M. F. Wever, PharmD;
Thomas F. Lüscher, MD;
Francesco Cosentino, MD;
; Ton J. Rabelink, MD
From the Departments of Clinical Chemistry (R.M.F.W.) and Nephrology and
Hypertension (T.J.R.), University Hospital Utrecht, the Netherlands, and
Cardiology, University Hospital Zurich and Cardiovascular Research, Institute
of Physiology, University of Zürich, Switzerland (T.F.L.), and
I.R.C.C.S., Neromed Pozzilli, Italy.
Correspondence to Ton. J. Rabelink, MD, PhD, Department of Nephrology and Hypertension, University Hospital Utrecht, Room F03.226, PO Box 85500, 3508 GA Utrecht, Netherlands. E-mail T.Rabelink@digd.azu.nl
Key Words: endothelium-derived factors • atherosclerosis • endothelium
 |
Introduction
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Nitric
oxide is a principal factor involved in the antiatherosclerotic
properties of the
endothelium.1 2 3 NO interferes in
vitro with key events in the development of
atherosclerosis, such as monocyte and leukocyte
adhesion to the endothelium4 5 6 7
as well as platelet–vessel wall
interaction.8 9 10 NO also decreases
endothelial permeability and reduces vessel tone, thus
decreasing flux of lipoproteins into the vessel
wall.11 12 Finally, NO has been shown to inhibit
vascular smooth muscle cell proliferation and migration in vitro as
well as in vivo.13 14 15 16 In agreement with these
findings, inhibition of the NO-producing enzyme NOS III caused
accelerated atherosclerosis in experimental
models.17 Major risk factors for atherosclerotic
vascular disease, such as hypercholesterolemia,
diabetes, hypertension, and smoking, have been associated with impaired
NO activity.18 19 20 21 22
In vivo, the activity of the L-arginine–NO pathway is a
balance between the synthesis and breakdown of NO. At present,
there are several reasons to believe that NO synthesis could indeed be
impaired in hypercholesterolemia and
atherosclerosis. In these conditions, there appears to
be an uncoupling of the receptor-Gi
complex.23 The exact mechanism is not known, but
a very intriguing hypothesis is that the altered lipid composition of
the cell membrane may play a role in this phenomenon. Although there is
some controversy regarding the effect of oxidized LDL on the
transcription of the enzyme, there is evidence of reduced transcription
and enhanced breakdown of NOS transcripts with increasing
concentrations of oxidized LDL.24 Long-term
stimulation with oxidized LDL may also lead to a decrease in the amount
of the NOS . . . [Full Text of this Article]
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