Oxidized low-density lipoproteins increase arginase activity and reciprocally decrease
endothelial NO in human aortic endothelial cells. Here, we demonstrate that vascular …

Oxidized low-density lipoprotein (OxLDL) impairs NO signaling and endothelial function,
and contributes to the pathogenesis of atherosclerosis. Arginase reciprocally regulates NO …

Arginase can cause vascular dysfunction by competing with nitric oxide synthase for l-
arginine and by increasing cell proliferation and collagen formation, which promote vascular …

Decreased endothelial nitric oxide (NO) bioavailability as it relates to endothelial dysfunction
plays an important role in various cardiovascular disorders, including atherosclerosis …

Background—Arginase competes with endothelial nitric oxide synthase (eNOS) for the
substrate l-arginine and decreases NO production. This study investigated regulatory …

Aims Elevation of arginase activity has been linked to vascular dysfunction in diabetes and
hypertension by a mechanism involving decreased nitric oxide (NO) bioavailability due to L …

Background—Although abnormal l-arginine NO signaling contributes to endothelial
dysfunction in the aging cardiovascular system, the biochemical mechanisms remain …

Arginase, expressed in endothelial cells and upregulated in aging blood vessels, competes
with NO synthase (NOS) for l-arginine, thus modulating vasoreactivity and attenuating NO …

Endothelial dysfunction represents an early change in the vascular wall in areas prone to
atherosclerotic plaque formation and is present in association with several risk factors for …

Arginase metabolizes the semi-essential amino acid l-arginine to l-ornithine and urea. There
are two distinct isoforms of arginase, arginase I and II, which are encoded by separate …