Enhanced vascular arginase activity impairs endothelium-dependent vasorelaxation by
decreasing l-arginine availability to endothelial nitric oxide (NO) synthase, thereby reducing …

Enhanced vascular arginase activity can impair endothelium-dependent vasorelaxation by
decreasing l-arginine availability to endothelial nitric oxide (NO) synthase, thereby reducing …

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 …

Reduced nitric oxide bioavailability contributes to increased cardiovascular disease risk in
patients with chronic kidney disease (CKD). Arginase has been implicated as a potential …

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

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

Functional integrity of the vascular endothelium is of fundamental importance for normal
vascular function. A key factor regulating endothelial function is the bioavailability of nitric …

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

The incidence of cardiovascular disease is predicted to increase as the population ages.
There is accumulating evidence that arginase upregulation is associated with impaired …

Reduced production of nitric oxide (NO) is one of the first indications of endothelial
dysfunction and precedes overt cardiovascular disease. Increased expression of Arginase …