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ADMA and oxidative stress are responsible for endothelial dysfunction in hyperhomocyst(e)inemia: effects of L-arginine and B vitamins.

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ADMA and oxidative stress are responsible for endothelial dysfunction in hyperhomocyst(e)inemia: effects of L-arginine and B vitamins. / Sydow, Karsten; Schwedhelm, Edzard; Arakawa, Naoshi; Bode-Böger, Stefanie M; Tsikas, Dimitrios; Hornig, Burkhard; Frölich, Jürgen C; Böger, Rainer H.

In: CARDIOVASC RES, Vol. 57, No. 1, 1, 2003, p. 244-252.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Sydow, K, Schwedhelm, E, Arakawa, N, Bode-Böger, SM, Tsikas, D, Hornig, B, Frölich, JC & Böger, RH 2003, 'ADMA and oxidative stress are responsible for endothelial dysfunction in hyperhomocyst(e)inemia: effects of L-arginine and B vitamins.', CARDIOVASC RES, vol. 57, no. 1, 1, pp. 244-252. <http://www.ncbi.nlm.nih.gov/pubmed/12504835?dopt=Citation>

APA

Sydow, K., Schwedhelm, E., Arakawa, N., Bode-Böger, S. M., Tsikas, D., Hornig, B., Frölich, J. C., & Böger, R. H. (2003). ADMA and oxidative stress are responsible for endothelial dysfunction in hyperhomocyst(e)inemia: effects of L-arginine and B vitamins. CARDIOVASC RES, 57(1), 244-252. [1]. http://www.ncbi.nlm.nih.gov/pubmed/12504835?dopt=Citation

Vancouver

Sydow K, Schwedhelm E, Arakawa N, Bode-Böger SM, Tsikas D, Hornig B et al. ADMA and oxidative stress are responsible for endothelial dysfunction in hyperhomocyst(e)inemia: effects of L-arginine and B vitamins. CARDIOVASC RES. 2003;57(1):244-252. 1.

Bibtex

@article{dae19aa2cc9c466083f5812904cccc4c,
title = "ADMA and oxidative stress are responsible for endothelial dysfunction in hyperhomocyst(e)inemia: effects of L-arginine and B vitamins.",
abstract = "OBJECTIVES: Hyperhomocyst(e)inemia is a risk factor for atherosclerotic vascular disease, and it is associated with endothelial dysfunction. Mechanisms responsible for endothelial dysfunction in hyperhomocyst(e)inemia may involve impaired bioavailability of NO, possibly secondary to accumulation of the endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) and increased oxidative stress. We investigated whether oral treatment with B vitamins or L-arginine normalizes endothelium-dependent, flow-dependent vasodilation (FDD) in patients with peripheral arterial occlusive disease (PAOD) and hyperhomocyst(e)inemia. METHODS: 27 patients with PAOD and hyperhomocyst(e)inemia were assigned to oral treatment with combined B vitamins (folate, 10 mg; vitamin B-12, 200 microg; vitamin B-6, 20 mg/day), L-arginine (24 g/day) or placebo, for 8 weeks in a double-blind fashion. FDD was determined by high-resolution ultrasound in the radial artery. RESULTS: Vitamin B supplementation significantly lowered plasma homocyst(e)ine concentration from 15.8+/-1.8 to 8.7+/-1.1 micromol/l (P",
author = "Karsten Sydow and Edzard Schwedhelm and Naoshi Arakawa and Bode-B{\"o}ger, {Stefanie M} and Dimitrios Tsikas and Burkhard Hornig and Fr{\"o}lich, {J{\"u}rgen C} and B{\"o}ger, {Rainer H}",
year = "2003",
language = "Deutsch",
volume = "57",
pages = "244--252",
journal = "CARDIOVASC RES",
issn = "0008-6363",
publisher = "Oxford University Press",
number = "1",

}

RIS

TY - JOUR

T1 - ADMA and oxidative stress are responsible for endothelial dysfunction in hyperhomocyst(e)inemia: effects of L-arginine and B vitamins.

AU - Sydow, Karsten

AU - Schwedhelm, Edzard

AU - Arakawa, Naoshi

AU - Bode-Böger, Stefanie M

AU - Tsikas, Dimitrios

AU - Hornig, Burkhard

AU - Frölich, Jürgen C

AU - Böger, Rainer H

PY - 2003

Y1 - 2003

N2 - OBJECTIVES: Hyperhomocyst(e)inemia is a risk factor for atherosclerotic vascular disease, and it is associated with endothelial dysfunction. Mechanisms responsible for endothelial dysfunction in hyperhomocyst(e)inemia may involve impaired bioavailability of NO, possibly secondary to accumulation of the endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) and increased oxidative stress. We investigated whether oral treatment with B vitamins or L-arginine normalizes endothelium-dependent, flow-dependent vasodilation (FDD) in patients with peripheral arterial occlusive disease (PAOD) and hyperhomocyst(e)inemia. METHODS: 27 patients with PAOD and hyperhomocyst(e)inemia were assigned to oral treatment with combined B vitamins (folate, 10 mg; vitamin B-12, 200 microg; vitamin B-6, 20 mg/day), L-arginine (24 g/day) or placebo, for 8 weeks in a double-blind fashion. FDD was determined by high-resolution ultrasound in the radial artery. RESULTS: Vitamin B supplementation significantly lowered plasma homocyst(e)ine concentration from 15.8+/-1.8 to 8.7+/-1.1 micromol/l (P

AB - OBJECTIVES: Hyperhomocyst(e)inemia is a risk factor for atherosclerotic vascular disease, and it is associated with endothelial dysfunction. Mechanisms responsible for endothelial dysfunction in hyperhomocyst(e)inemia may involve impaired bioavailability of NO, possibly secondary to accumulation of the endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA) and increased oxidative stress. We investigated whether oral treatment with B vitamins or L-arginine normalizes endothelium-dependent, flow-dependent vasodilation (FDD) in patients with peripheral arterial occlusive disease (PAOD) and hyperhomocyst(e)inemia. METHODS: 27 patients with PAOD and hyperhomocyst(e)inemia were assigned to oral treatment with combined B vitamins (folate, 10 mg; vitamin B-12, 200 microg; vitamin B-6, 20 mg/day), L-arginine (24 g/day) or placebo, for 8 weeks in a double-blind fashion. FDD was determined by high-resolution ultrasound in the radial artery. RESULTS: Vitamin B supplementation significantly lowered plasma homocyst(e)ine concentration from 15.8+/-1.8 to 8.7+/-1.1 micromol/l (P

M3 - SCORING: Zeitschriftenaufsatz

VL - 57

SP - 244

EP - 252

JO - CARDIOVASC RES

JF - CARDIOVASC RES

SN - 0008-6363

IS - 1

M1 - 1

ER -