Arginine and Endothelial Function

Abstract

Arginine (L-arginine), is an amino acid involved in a number of biological processes, including the biosynthesis of proteins, host immune response, urea cycle, and nitric oxide production. In this systematic review, we focus on the functional role of arginine in the regulation of endothelial function and vascular tone. Both clinical and preclinical studies are examined, analyzing the effects of arginine supplementation in hypertension, ischemic heart disease, aging, peripheral artery disease, and diabetes mellitus.

Effects of Chronic Supplementation of L‐Arginine on Physical Fitness in Water Polo Players

“…In this scenario, the L-Arginine vasodilator effect has gained the favor of the athletes to improve their physical performance [ 14 , 21 , 26 ]. The perceived benefit of L-Arginine assumption, though, ailments the described arginine paradox, which has been described by Ignarro and coworkers; indeed, L-Arginine is a nonessential amino acid, synthesized in the small intestine from proline, glutamate, and glutamine, which is also abundant in diets with apparently no need for supplementation [ 27 – 29 ].…”

Plasma Metabolomic Profiles Differentiate Patients With Dilated Cardiomyopathy and Ischemic Cardiomyopathy

“…The therapeutic strategy regarding glutamine and glutamate metabolism may be considered in future personalized treatment for ICM. Furthermore, Arginine biosynthesis, involved in a number of biological processes, including the biosynthesis of proteins, host immune response, urea cycle, and nitric oxide production, plays an important role in the regulation of endothelial function and vascular tone, which is vital for ICM treatment (23,49). alpha-linolenic acid metabolism was observed in both DCM and ICM, but it found to be significant only in DCM group.…”

Cystathionine γ-lyase promotes estrogen-stimulated uterine artery blood flow via glutathione homeostasis

“…6 A). Arginine stimulates NO-dependent vasodilation [ 2 ], whereas urea cycle arginase competes with NO synthases for arginine, thereby decreasing NO x [ 48 ]. Altered abundance of these amino acids could therefore indicate differential urea cycle or eNOS activity.…”

“…CSE regulation of amino acid metabolism may facilitate NO-stimulated UBF. Decreased arginine availability for NO synthesis is a key mechanism of endothelial dysfunction, which may be due to increased endogenous eNOS inhibitors, greater urea cycle activity, or decreased eNOS expression or eNOS S1177 phosphorylation [ 1 , 2 ]. In our model, similar WT and CSE KO serum arginine and ornithine levels suggest comparable urea cycle activity.…”

“…Estrogen (17β-estradiol; E 2 ) regulates uterine artery blood flow (UBF) via the gasotransmitter nitric oxide (NO) [ 1 ]. Following menses and during pregnancy, rising E 2 levels activate endothelial NO synthase (eNOS) to produce NO from arginine [ 1 , 2 ]. NO stimulates the soluble guanylate cyclase (sGC)-protein kinase G (PKG) pathway, which promotes relaxation of vascular myocytes and causes vasodilation and increased blood flow [ [3] , [4] , [5] , [6] , [7] ].…”