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Asymmetric dimethylarginine, oxidative stress, and vascular nitric oxide synthase in essential hypertension

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Standard

Asymmetric dimethylarginine, oxidative stress, and vascular nitric oxide synthase in essential hypertension. / Wang, Dan; Strandgaard, Svend; Iversen, Jens; Wilcox, Christopher S.

I: American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, Bind 296, Nr. 2, 2009, s. R195-200.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Wang, D, Strandgaard, S, Iversen, J & Wilcox, CS 2009, 'Asymmetric dimethylarginine, oxidative stress, and vascular nitric oxide synthase in essential hypertension', American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, bind 296, nr. 2, s. R195-200. https://doi.org/10.1152/ajpregu.90506.2008

APA

Wang, D., Strandgaard, S., Iversen, J., & Wilcox, C. S. (2009). Asymmetric dimethylarginine, oxidative stress, and vascular nitric oxide synthase in essential hypertension. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, 296(2), R195-200. https://doi.org/10.1152/ajpregu.90506.2008

Vancouver

Wang D, Strandgaard S, Iversen J, Wilcox CS. Asymmetric dimethylarginine, oxidative stress, and vascular nitric oxide synthase in essential hypertension. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology. 2009;296(2):R195-200. https://doi.org/10.1152/ajpregu.90506.2008

Author

Wang, Dan ; Strandgaard, Svend ; Iversen, Jens ; Wilcox, Christopher S. / Asymmetric dimethylarginine, oxidative stress, and vascular nitric oxide synthase in essential hypertension. I: American Journal of Physiology: Regulatory, Integrative and Comparative Physiology. 2009 ; Bind 296, Nr. 2. s. R195-200.

Bibtex

@article{ff18f560367a11df8ed1000ea68e967b,
title = "Asymmetric dimethylarginine, oxidative stress, and vascular nitric oxide synthase in essential hypertension",
abstract = "We reported impaired endothelium-derived relaxation factor/nitric oxide (EDRF/NO) responses and constitutive nitric oxide synthase (cNOS) activity in subcutaneous vessels dissected from patients with essential hypertension (n = 9) compared with normal controls (n = 10). We now test the hypothesis that the patients in this study have increased circulating levels of the cNOS inhibitor, asymmetric dimethylarginine (ADMA), or the lipid peroxidation product of linoleic acid, 13-hydroxyoctadecadienoic acid (HODE), which is a marker of reactive oxygen species. Patients had significantly (P < 0.001) elevated (means +/- SD) plasma levels of ADMA (P(ADMA), 766 +/- 217 vs. 393 +/- 57 nmol/l) and symmetric dimethylarginine (P(SDMA): 644 +/- 140 vs. 399 +/- 70 nmol/l) but similar levels of L-arginine accompanied by significantly (P < 0.015) increased rates of renal ADMA excretion (21 +/- 9 vs. 14 +/- 5 nmol/mumol creatinine) and decreased rates of renal ADMA clearance (18 +/- 3 vs. 28 +/- 5 ml/min). They had significantly increased plasma levels of HODE (P(HODE): 309 +/- 30 vs. 226 +/- 24 nmol/l) and renal HODE excretion (433 +/- 93 vs. 299 +/- 67 nmol/micromol creatinine). For the combined group of normal and hypertensive subjects, the individual values for plasma levels of ADMA and HODE were both significantly (P < 0.001) and inversely correlated with microvascular EDRF/NO and positively correlated with mean blood pressure. In conclusion, elevated levels of ADMA and oxidative stress in a group of hypertensive patients could contribute to the associated microvascular endothelial dysfunction and elevated blood pressure.",
author = "Dan Wang and Svend Strandgaard and Jens Iversen and Wilcox, {Christopher S}",
note = "Keywords: Adult; Arginine; Blood Pressure; Buttocks; Endothelium-Dependent Relaxing Factors; Female; Humans; Hypertension; Linoleic Acids; Lipid Peroxidation; Male; Microvessels; Middle Aged; Nitric Oxide; Nitric Oxide Synthase; Oxidative Stress; Subcutaneous Tissue; Up-Regulation; Vasodilation; Young Adult",
year = "2009",
doi = "10.1152/ajpregu.90506.2008",
language = "English",
volume = "296",
pages = "R195--200",
journal = "American Journal of Physiology: Regulatory, Integrative and Comparative Physiology",
issn = "0363-6119",
publisher = "American Physiological Society",
number = "2",

}

RIS

TY - JOUR

T1 - Asymmetric dimethylarginine, oxidative stress, and vascular nitric oxide synthase in essential hypertension

AU - Wang, Dan

AU - Strandgaard, Svend

AU - Iversen, Jens

AU - Wilcox, Christopher S

N1 - Keywords: Adult; Arginine; Blood Pressure; Buttocks; Endothelium-Dependent Relaxing Factors; Female; Humans; Hypertension; Linoleic Acids; Lipid Peroxidation; Male; Microvessels; Middle Aged; Nitric Oxide; Nitric Oxide Synthase; Oxidative Stress; Subcutaneous Tissue; Up-Regulation; Vasodilation; Young Adult

PY - 2009

Y1 - 2009

N2 - We reported impaired endothelium-derived relaxation factor/nitric oxide (EDRF/NO) responses and constitutive nitric oxide synthase (cNOS) activity in subcutaneous vessels dissected from patients with essential hypertension (n = 9) compared with normal controls (n = 10). We now test the hypothesis that the patients in this study have increased circulating levels of the cNOS inhibitor, asymmetric dimethylarginine (ADMA), or the lipid peroxidation product of linoleic acid, 13-hydroxyoctadecadienoic acid (HODE), which is a marker of reactive oxygen species. Patients had significantly (P < 0.001) elevated (means +/- SD) plasma levels of ADMA (P(ADMA), 766 +/- 217 vs. 393 +/- 57 nmol/l) and symmetric dimethylarginine (P(SDMA): 644 +/- 140 vs. 399 +/- 70 nmol/l) but similar levels of L-arginine accompanied by significantly (P < 0.015) increased rates of renal ADMA excretion (21 +/- 9 vs. 14 +/- 5 nmol/mumol creatinine) and decreased rates of renal ADMA clearance (18 +/- 3 vs. 28 +/- 5 ml/min). They had significantly increased plasma levels of HODE (P(HODE): 309 +/- 30 vs. 226 +/- 24 nmol/l) and renal HODE excretion (433 +/- 93 vs. 299 +/- 67 nmol/micromol creatinine). For the combined group of normal and hypertensive subjects, the individual values for plasma levels of ADMA and HODE were both significantly (P < 0.001) and inversely correlated with microvascular EDRF/NO and positively correlated with mean blood pressure. In conclusion, elevated levels of ADMA and oxidative stress in a group of hypertensive patients could contribute to the associated microvascular endothelial dysfunction and elevated blood pressure.

AB - We reported impaired endothelium-derived relaxation factor/nitric oxide (EDRF/NO) responses and constitutive nitric oxide synthase (cNOS) activity in subcutaneous vessels dissected from patients with essential hypertension (n = 9) compared with normal controls (n = 10). We now test the hypothesis that the patients in this study have increased circulating levels of the cNOS inhibitor, asymmetric dimethylarginine (ADMA), or the lipid peroxidation product of linoleic acid, 13-hydroxyoctadecadienoic acid (HODE), which is a marker of reactive oxygen species. Patients had significantly (P < 0.001) elevated (means +/- SD) plasma levels of ADMA (P(ADMA), 766 +/- 217 vs. 393 +/- 57 nmol/l) and symmetric dimethylarginine (P(SDMA): 644 +/- 140 vs. 399 +/- 70 nmol/l) but similar levels of L-arginine accompanied by significantly (P < 0.015) increased rates of renal ADMA excretion (21 +/- 9 vs. 14 +/- 5 nmol/mumol creatinine) and decreased rates of renal ADMA clearance (18 +/- 3 vs. 28 +/- 5 ml/min). They had significantly increased plasma levels of HODE (P(HODE): 309 +/- 30 vs. 226 +/- 24 nmol/l) and renal HODE excretion (433 +/- 93 vs. 299 +/- 67 nmol/micromol creatinine). For the combined group of normal and hypertensive subjects, the individual values for plasma levels of ADMA and HODE were both significantly (P < 0.001) and inversely correlated with microvascular EDRF/NO and positively correlated with mean blood pressure. In conclusion, elevated levels of ADMA and oxidative stress in a group of hypertensive patients could contribute to the associated microvascular endothelial dysfunction and elevated blood pressure.

U2 - 10.1152/ajpregu.90506.2008

DO - 10.1152/ajpregu.90506.2008

M3 - Journal article

C2 - 18685064

VL - 296

SP - R195-200

JO - American Journal of Physiology: Regulatory, Integrative and Comparative Physiology

JF - American Journal of Physiology: Regulatory, Integrative and Comparative Physiology

SN - 0363-6119

IS - 2

ER -

ID: 18788474