Reduced Urinary Excretion of Nitric Oxide Metabolites and Increased Plasma Levels of Asymmetric Dimethylarginine in Men with Essential Hypertension

1999 ◽  
Vol 33 (4) ◽  
pp. 652-658 ◽  
Author(s):  
Andrzej Surdacki ◽  
Michał Nowicki ◽  
Joerg Sandmann ◽  
Dimitrios Tsikas ◽  
Rainer H. Boeger ◽  
...  
2009 ◽  
Vol 296 (2) ◽  
pp. R195-R200 ◽  
Author(s):  
Dan Wang ◽  
Svend Strandgaard ◽  
Jens Iversen ◽  
Christopher S. Wilcox

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 (PADMA, 766 ± 217 vs. 393 ± 57 nmol/l) and symmetric dimethylarginine (PSDMA: 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/μmol creatinine) and decreased rates of renal ADMA clearance (18 ± 3 vs. 28 ± 5 ml/min). They had significantly increased plasma levels of HODE (PHODE: 309 ± 30 vs. 226 ± 24 nmol/l) and renal HODE excretion (433 ± 93 vs. 299 ± 67 nmol/μmol 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.


1996 ◽  
Vol 52 (9) ◽  
pp. 1447-1451 ◽  
Author(s):  
Jan G.C. van Amsterdam ◽  
Cees van den Berg ◽  
Jetske Zuidema ◽  
Jan-Dirk te Biesebeek ◽  
Hartmut Rokos

2013 ◽  
Vol 258 (6) ◽  
pp. 1072-1078 ◽  
Author(s):  
Jaap W. Hol ◽  
Felix van Lier ◽  
Madelous Valk ◽  
Markus Klimek ◽  
Robert J. Stolker ◽  
...  

2015 ◽  
Vol 65 (10) ◽  
pp. A825
Author(s):  
Lien Trieu ◽  
Payman Zamani ◽  
Paschalis-Thomas Doulias ◽  
Deepa Rawat ◽  
Prithvi Shiva Kumar ◽  
...  

2001 ◽  
Vol 101 (1) ◽  
pp. 73-78 ◽  
Author(s):  
Ernesto BRAGULAT ◽  
Alejandro de la SIERRA ◽  
María T. ANTONIO ◽  
Wladimiro JIMÉNEZ ◽  
Álvaro URBANO-MÁRQUEZ ◽  
...  

The aim of the present study was to evaluate the effects of the level of salt intake on endothelium-derived factors in a group of patients with essential hypertension. A group of 50 patients with essential hypertension who had never been treated for the condition were placed on a low-sodium (50 mmol/day), low-nitrate (400 µmol/day) diet, which was supplemented, in a single-blind fashion, with placebo tablets for the first 7 days and then with NaCl tablets (200 mmol/day) for a further 7 days (total sodium intake 250 mmol/day). At the end of both periods, 24-h ambulatory blood pressure monitoring was performed. In addition, plasma levels and 24-h urinary excretion of nitrites plus nitrates and cGMP were measured, along with plasma levels of endothelin. A high salt intake promoted significant decreases in plasma levels of nitrites plus nitrates (from 41.0±2.1 to 32.8±1.8 nmol/ml; P < 0.001), 24-h urinary nitrate excretion (from 417±36 to 334±37 µmol/24 h; P = 0.045) and plasma endothelin levels (from 5.6±0.3 to 4.6±0.3 pg/ml; P = 0.007). The plasma concentration and 24-h urinary excretion of cGMP were not altered significantly by a high salt intake. We did not find any relationship between endothelium-derived products and 24-h mean blood pressure, at either low or high salt intakes, or between changes induced by the high-salt diet. A high salt intake also induced significant decreases in plasma renin activity, angiotensin II and aldosterone, and a significant increase in atrial natriuretic peptide. We conclude that a high salt intake decreases the plasma concentration and urinary excretion of nitrates and plasma levels of endothelin in patients with essential hypertension, suggesting that the level of salt intake may affect endothelial cell function. However, these alterations are not correlated with changes in blood pressure induced by the high salt intake.


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