Hypertension. 1998;31:1047-1060
(Hypertension. 1998;31:1047-1060.)
© 1998 American Heart Association, Inc.
Review of Alterations in Endothelial Nitric Oxide Production in Diabetes
Protective Role of Arginine on Endothelial Dysfunction
Galen M. Pieper
From the Department of Transplant Surgery, Medical College of Wisconsin,
Froedtert Memorial Hospital (Milwaukee).
Correspondence to Dr Galen M. Pieper, Department of Transplant Surgery, Medical College of Wisconsin, Froedtert Memorial Hospital, 9200 W Wisconsin Ave, Milwaukee, WI 53226. E-mail gmpieper@pot.its.mcw.edu
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Introduction
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Nitric
oxide release from the endothelium plays an important
role in regulation of vascular tone,1 inhibition
of both platelet and leukocyte aggregation and
adhesion,1 2 and inhibition of cell
proliferation.3 These properties suggest that the
level of NO production by the endothelium may
play a pivotal role in the regulation of vascular disease.
Analysis using mass spectrometry has revealed that NO is
produced by NOS from the terminal guanidino nitrogen of the precursor
amino acid L-arginine.4 Thus,
utilization of L-arginine and conversion to NO may
establish a regulatory site in the development of
endothelial dysfunction.
Endothelial dysfunction is characterized by defective
endothelium-dependent relaxation, and some reviews
regarding endothelial dysfunction in diabetes have been
published.5 6 7 8 These reviews have focused on
factors that might contribute to defective relaxation, some of which
will not be addressed in detail in this review. The purpose of the
present review is to summarize evidence that specifically supports
either decreased NO production by diabetic vascular
endothelium and/or impaired NO-mediated
endothelium-dependent relaxation. Second, this review
provides reasonable alternatives to explain some of the controversies
in this research area. Third, since there is growing evidence that
arginine appears to have some benefits for diabetes-associated
abnormalities, this review summarizes the current state of knowledge of
effects of acute and chronic administration of L-arginine
on diabetes-induced endothelial dysfunction and
discusses potential NO-dependent and -independent mechanisms whereby
therapeutic intervention with L-arginine might benefit the
diabetic endothelium.
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Impaired Endothelium-Dependent Relaxation
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Experimental Diabetes Mellitus
Decreases in endothelium-dependent relaxation are
a common feature in both conduit9 10 11 12 13 14 15 16 17 18 19 20 and
resistance21 22 23 24 25 26 27 28 29 30 . . . [Full Text of this Article]
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