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Physiological Reviews, Vol. 83, No. 1, January 2003, pp. 183-252; 10.1152/physrev.00022.2002.
Copyright ©2003 by the American Physiological Society
Centre for Cardiovascular Biology and Medicine, Guy's, King's, and St. Thomas' School of Biomedical Sciences, King's College London, London, United Kingdom; Programa de Fisiologia y Biofisica, Instituto de Ciencias Biomedicas, Universidad de Chile, Santiago; and Cellular and Molecular Physiology Laboratory, Department of Physiology, Faculty of Biological Sciences, University of Concepción, Concepción, Chile
Mann, Giovanni E.,
David L. Yudilevich, and
Luis Sobrevia.
Regulation of Amino Acid and Glucose Transporters in
Endothelial and Smooth Muscle Cells. Physiol. Rev. 83: 183-252, 2003.
While transport processes for amino acids
and glucose have long been known to be expressed in the luminal and
abluminal membranes of the endothelium comprising the blood-brain
and blood-retinal barriers, it is only within the last decades that
endothelial and smooth muscle cells derived from peripheral vascular
beds have been recognized to rapidly transport and metabolize these nutrients. This review focuses principally on the mechanisms regulating amino acid and glucose transporters in vascular endothelial cells, although we also summarize recent advances in the understanding of the
mechanisms controlling membrane transport activity and expression in
vascular smooth muscle cells. We compare the specificity, ionic
dependence, and kinetic properties of amino acid and glucose transport
systems identified in endothelial cells derived from cerebral, retinal,
and peripheral vascular beds and review the regulation of transport by
vasoactive agonists, nitric oxide (NO), substrate deprivation, hypoxia,
hyperglycemia, diabetes, insulin, steroid hormones, and development. In
view of the importance of NO as a modulator of vascular tone under
basal conditions and in disease and chronic inflammation, we critically
review the evidence that transport of L-arginine and
glucose in endothelial and smooth muscle cells is modulated by
bacterial endotoxin, proinflammatory cytokines, and atherogenic lipids.
The recent colocalization of the cationic amino acid transporter CAT-1
(system y+), nitric oxide synthase (eNOS), and caveolin-1
in endothelial plasmalemmal caveolae provides a novel mechanism for the
regulation of NO production by L-arginine delivery and
circulating hormones such insulin and 17
-estradiol.
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