Angiotensin converting enzyme inhibition and angiotensin II AT1-receptor blockade reduce the levels of asymmetrical NG, NG-dimethylarginine in human essential hypertension

被引:131
作者
Delles, C
Schneider, MP
John, S
Gekle, M
Schmieder, RE
机构
[1] Univ Erlangen Nurnberg, Klinikum Nurnberg Sud, Dept Med Nephrol, D-90471 Nurnberg, Germany
[2] Univ Wurzburg, Dept Physiol, D-8700 Wurzburg, Germany
关键词
endothelium; endothelium-derived factors; hypertension; angiotensin-converting enzyme; angiotensin antagonist;
D O I
10.1016/S0895-7061(02)02278-1
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Background: Asymmetrical N-G, N-G-dimethylarginine (ADMA) is associated with impaired endothelium-dependent vasodilation in humans. Methods: Twenty young, male. mildly hypertensive subjects were included in a randomized. double-blind, fourfold cross-over study with placebo, enalapril (20 mg/day), eprosartan (600 mg/day). or a combination of both drugs (10 and 300 mg/day. respectively) each over 1 week, followed by a 2-week wash-out phase. After each treatment phase, ADMA concentration was measured. Results: ADMA concentration was 1.69 +/- 0.59 mumol/L in the placebo phase, and was significantly lower in the enalapril. eprosartan. and combination phases (1.41 +/- 0.29, 1.42 +/- 0.43, and 1.38 +/- 0.30 mumol/L. respectively all P < 0.05 v placebo). Changes in ADMA levels were independent of the drugs' action on blood pressure (BP). Conclusions: Levels of ADMA were reduced with enalapril and eprosartan therapy. Our results suggest a specific action of these drugs on ADMA levels that is independent of BP. (C) 2002 American Journal of Hypertension, Ltd.
引用
收藏
页码:590 / 593
页数:4
相关论文
共 13 条
[1]   Asymmetric dimethylarginine (ADMA):: A novel risk factor for endothelial dysfunction -: Its role in hypercholesterolemia [J].
Böger, RH ;
Bode-Böger, SM ;
Szuba, A ;
Tsao, PS ;
Chan, JR ;
Tangphao, O ;
Blaschke, TF ;
Cooke, JP .
CIRCULATION, 1998, 98 (18) :1842-1847
[2]   LDL cholesterol upregulates synthesis of asymmetrical dimethylarginine in human endothelial cells -: Involvement of S-adenosylmethionine-dependent methyltransferases [J].
Böger, RH ;
Sydow, K ;
Borlak, J ;
Thum, T ;
Lenzen, H ;
Schubert, B ;
Tsikas, D ;
Bode-Böger, SM .
CIRCULATION RESEARCH, 2000, 87 (02) :99-105
[3]  
CALVER A, 1993, J HUM HYPERTENS, V7, P193
[4]  
Carey RM, 2000, ACTA PHYSIOL SCAND, V168, P65
[5]   Does ADMA cause endothelial dysfunction? [J].
Cooke, JP .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2000, 20 (09) :2032-2037
[6]   Nitric oxide synthase inhibitors and hypertension in children and adolescents [J].
Goonasekera, CDA ;
Rees, DD ;
Woolard, P ;
Frend, A ;
Shah, V ;
Dillon, MJ .
JOURNAL OF HYPERTENSION, 1997, 15 (08) :901-909
[7]   Novel mechanism for endothelial dysfunction - Dysregulation of dimethylarginine dimethylaminohydrolase [J].
Ito, A ;
Tsao, PS ;
Adimoolam, S ;
Kimoto, M ;
Ogawa, T ;
Cooke, JP .
CIRCULATION, 1999, 99 (24) :3092-3095
[8]  
Mancini GBJ, 2000, CLIN INVEST MED, V23, P144
[9]   Acute and chronic angiotensin-1 receptor antagonism reverses endothelial dysfunction in atherosclerosis [J].
Prasad, A ;
Tupas-Habib, T ;
Schenke, WH ;
Mincemoyer, R ;
Panza, JA ;
Waclawin, MA ;
Ellahham, S ;
Quyyumi, AA .
CIRCULATION, 2000, 101 (20) :2349-2354
[10]  
Schlaich MP, 1998, CLIN NEPHROL, V49, P153