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L-Arginine, Nitric Oxide, and Endothelial Dysfunction Underlying Atherosclerotic

Cardiovascular Disease (ASCVD)

J Atheroscler Thromb, 2023; 30:3


Endothelial Dysfunction and ASCVD A growing number of evidence suggests that endothelial dysfunction is associated with cardiovascular events1, 2). Nitric oxide (NO) plays a significant role in the maintenance of vascular endothelial function by inhibiting vasoconstriction, vascular smooth muscle cell proliferation, leukocyte adhesion, and platelet aggregation. As the concept that endothelial dysfunction may be regarded as the integrated risk of the risk factors and serves as a sensitive marker for their functional significance, the development and introduction of novel, cost-effective, noninvasive, and reproducible tests to assess endothelial function may conceivably promote the use of these tests for clinical application and practice1,2.

L-arginine has received much interest during the past two decades because of its potential effects on whole-body NO production and the augmentation of NO-dependent signaling pathways. L-arginine is a source of nitrogen, which is converted to NO by eNOS ( endothelial NO synthase) and is involved in maintaining vascular function. Therefore, decreased L-arginine use can be involved in vascular endothelial damage owing to NO bioavailability. Even with normal L-arginine levels, vascular endothelial dysfunction may occur and is referred to as “arginine paradox”3). The global L-arginine bioavailability ratio (GABR) may be a better predictor of coronary artery disease than L-arginine, but its diagnostic potential has not been examined4). Ishinoda et al. reported that the L-arginine/L-ornithine ratio is a predictor of cardiovascular death in this issue 5).

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