The increase of vascular arginase activity during aging causes endothelial dysfunction. This
enzyme competes with the endothelial nitric oxide synthase (eNOS) for L-arginine substrate …

Objective—Arginase can reduce NO availability. In this study, we explored arginase as a
determinant of endothelial dysfunction in small arteries from obese patients and its …

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

There is increasing evidence that upregulation of arginase contributes to impaired
endothelial function in aging. In this study, we demonstrate that arginase upregulation leads …

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

Abstract Background Advanced glycation endproducts (AGEs) play a major role in the
development of many vascular complications that are mediated by endothelial dysfunction …

Background Cardiovascular disorders associated with endothelial dysfunction, such as
atherosclerosis, have decreased nitric oxide (NO) bioavailability. Arginase in the vasculature …

Reduced bioavailability of nitric oxide (NO) is accompanied by endothelial dysfunction,
which precedes clinical signs of atherosclerosis. The metalloenzyme arginase reciprocally …

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 …

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 …