Long-term oral administration of L-arginine reduces intimal thickening and enhances neoendothelium-dependent acetylcholine-induced relaxation after arterial injury.

Hamon, Martial; Vallet, B.; Bauters, Christophe; Wernert, Nicolas; McFadden, Eugène; Lablanche, Jean‐Marc; Dupuis, B; Bertrand, Michel E.

doi:10.1161/01.cir.90.3.1357

Cited by 113 publications

(60 citation statements)

References 25 publications

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“…NO production by VSMCs may in part compensate for the absence of endothelial NO synthesis by inhibiting smooth muscle cell proliferation, as well as by limiting thrombus formation by preventing platelet adhesion and aggregation. [35][36][37] This hypothesis is supported by the observation in animals that L-arginine attenuates neointimal formation after balloon injury 38 or that iNOS suppresses the development of allograft arteriosclerosis. 39 Thus, homocysteine-induced NO may suppress the atherothrombotic risk of hyperhomocysteinemic states.…”

Section: Discussionmentioning

confidence: 99%

Homocysteine Increases Nitric Oxide Synthesis in Cytokine-Stimulated Vascular Smooth Muscle Cells

Ikeda

Minota

et al. 1999

Circulation

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Background-Elevated plasma homocysteine levels have been reported to be an independent risk factor for vascular disease. However, there have been no reports concerning the effects of homocysteine on the production of nitric oxide (NO), another modulator of vascular function and proliferation, by the vascular smooth muscle. Methods and Results-We investigated the effects of homocysteine on NO synthesis by measuring the production of nitrite, a stable metabolite of NO, in cultured rat vascular smooth muscle cells (VSMCs). Incubation of cultures with interleukin (IL)-1␤ 10 ng/mL for 24 hours caused a significant increase in nitrite generation. The IL-1␤-induced nitrite production by VSMCs was significantly increased by homocysteine in a dose-dependent manner. This effect of homocysteine was significantly inhibited in the presence of N G -monomethyl-L-arginine or actinomycin D. The homocysteine-induced nitrite production was accompanied by increased inducible NO synthase mRNA and protein accumulation. Cysteine, glutathione, or hydrogen peroxide also increased nitrite accumulation in IL-1␤-stimulated VSMCs. Coincubation with the radical scavenger catalase or superoxide dismutase markedly reduced homocysteineinduced nitrite accumulation. Conclusions-Homocysteine

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Section: Discussionmentioning

confidence: 99%

Homocysteine Increases Nitric Oxide Synthesis in Cytokine-Stimulated Vascular Smooth Muscle Cells

Ikeda

Minota

et al. 1999

Circulation

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“…14 NO limits cytokine-induced endothelial activation 15,16 and modulates the expression of monocyte chemoattractant protein-1 in cultured endothelial cells 17 through a decrease in NF-B-binding activity. L-Arg decreases the adhesiveness of monocytes to the endothelium through inhibition of endothelium/leukocyte adhesion molecule transcription 18 ; L-arg limits the progression of atherosclerosis, 12,19 restores endothelium-dependent vasodilation, 20,21 and limits intimal proliferation of vascular smooth muscle cells after angioplasty. 21,22 We hypothesized that contact between atherosclerotic plaques and blood could increase TF expression by circulat-ing monocytes and that NO might limit this response.…”

mentioning

confidence: 99%

“…L-Arg decreases the adhesiveness of monocytes to the endothelium through inhibition of endothelium/leukocyte adhesion molecule transcription 18 ; L-arg limits the progression of atherosclerosis, 12,19 restores endothelium-dependent vasodilation, 20,21 and limits intimal proliferation of vascular smooth muscle cells after angioplasty. 21,22 We hypothesized that contact between atherosclerotic plaques and blood could increase TF expression by circulat-ing monocytes and that NO might limit this response. To test these hypotheses, we used a rabbit model of induced atherosclerosis (bilateral iliac injury and an atherogenic diet), and we performed angioplasty when atherosclerotic lesions were established.…”

mentioning

confidence: 99%

Enhanced Monocyte Tissue Factor Response After Experimental Balloon Angioplasty in Hypercholesterolemic Rabbit: Inhibition With Dietary l -Arginine

et al. 1998

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Background-There is evidence that tissue factor (TF) is a major contributor to the thrombogenicity of a ruptured atherosclerotic plaque. Nitric oxide (NO) has antiatherogenic and antithrombotic properties. We investigated whether L-arginine (L-arg), the endogenous precursor of NO, might affect the ability of monocytes to produce TF. Methods and Results-We studied TF expression in 18 rabbits with atherosclerosis induced by bilateral iliac damage and 10 weeks of a 2% cholesterol diet. Six weeks after the initiation of the diet, an angioplasty was performed. After angioplasty, the surviving rabbits (nϭ15) were randomized to receive L-arg (2.25%) supplementation in drinking water (L-arg group, nϭ8) or no treatment (untreated group, nϭ7). TF expression was evaluated in mononuclear cells from arterial blood in the presence and absence of endotoxin stimulation. Monocyte TF expression, as assessed with an amidolytic assay, did not differ significantly before or after the induction of atherosclerotic lesions (87Ϯ15 versus 70Ϯ12 mU of TF/1000 monocytes, PϭNS). Endotoxin-stimulated TF activity increased significantly 4 weeks after angioplasty (138Ϯ22 versus 70Ϯ12 mU of TF/1000 monocytes, Pϭ0.02). This increase was blunted by L-arg (43Ϯ16 mU of TF/1000 monocytes, Pϭ0.01). Conclusions-This study demonstrates that angioplasty-induced plaque rupture is associated with a marked increase in monocyte TF response that is blunted by the oral administration of L-arg. This suggests that the documented antithrombotic properties of NO may be related in part to an inhibitory effect on monocyte TF response. (Circulation. 1998;98:1776-1782.)

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“…Reducing nitric oxide availability through a synthase inhibitor (N G -nitro-Larginine methyl ester) increases the development of atherosclerosis, whereas increasing its availablity through the administration of L-arginine decreases its development, at least transiently. 17,18 These data suggest an important role for the endothelium in the prevention and promotion of atherosclerosis.…”

Section: See P 1234mentioning

confidence: 84%

Estrogens, Progestins, and Heart Disease

Vogel

Corretti

1998

Circulation

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Long-term oral administration of L-arginine reduces intimal thickening and enhances neoendothelium-dependent acetylcholine-induced relaxation after arterial injury.

Abstract: Our results demonstrate that L-arginine, a precursor of NO, reduces neointimal thickening after balloon denudation and improves neoendothelial-dependent acetylcholine-induced relaxation.

Cited by 113 publications

References 25 publications

Homocysteine Increases Nitric Oxide Synthesis in Cytokine-Stimulated Vascular Smooth Muscle Cells

Homocysteine Increases Nitric Oxide Synthesis in Cytokine-Stimulated Vascular Smooth Muscle Cells

Enhanced Monocyte Tissue Factor Response After Experimental Balloon Angioplasty in Hypercholesterolemic Rabbit: Inhibition With Dietary l -Arginine

Estrogens, Progestins, and Heart Disease

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