Targeting reactive oxygen species in hypertension

被引:40
作者
Delles, Christian [1 ]
Miller, William H. [1 ]
Dominiczak, Anna F. [1 ]
机构
[1] Univ Glasgow, BHF Glasgow Cardiovasc Res Ctr, Glasgow G12 8TA, Lanark, Scotland
基金
英国惠康基金;
关键词
D O I
10.1089/ars.2007.2008
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Oxidative stress plays an important role in the pathogenesis of hypertension. A number of sources of reactive oxygen species have been identified including NADPH oxidase, endothelial NO synthase, and xanthine oxidase. Inhibitors of these systems reduce blood pressure in experimental models. Targeted overexpression of antioxidant systems and interference with expression of oxidant systems has also been successfully used in animal models of hypertension. It is expected that these strategies will eventually be translated to human disease, but currently, the specificity and toxicity of such measures are not yet fulfilling quality criteria for treatment of humans. In the meantime, presumably nontoxic measures, such as administration of antioxidant vitamins, are the only available treatments for oxidative stress in humans. In this review, we discuss strategies to target oxidative stress both in experimental models and in humans. We also discuss how patients could be selected who particularly benefit from antioxidant treatment. In clinical practice, diagnostic procedures beyond measurement of blood pressure will be necessary to predict the response to antioxidants; these procedures will include measurement of antioxidant status and detailed assessment of vascular structure and function.
引用
收藏
页码:1061 / 1077
页数:17
相关论文
共 214 条
[1]   S-glutathiolation by peroxynitrite activates SERCA during arterial relaxation by nitric oxide [J].
Adachi, T ;
Weisbrod, RM ;
Pimentel, DR ;
Ying, J ;
Sharov, VS ;
Schöneich, C ;
Cohen, RA .
NATURE MEDICINE, 2004, 10 (11) :1200-1207
[2]   Targeting an antioxidant to mitochondria decreases cardiac ischemia-reperfusion injury [J].
Adlam, VJ ;
Harrison, JC ;
Porteous, CM ;
James, AM ;
Smith, RAJ ;
Murphy, MP ;
Sammut, IA .
FASEB JOURNAL, 2005, 19 (09) :1088-1095
[3]   Low-density lipoprotein cholesterol determines oxidative stress and endothelial dysfunction in saphenous veins from patients with coronary artery disease [J].
Al-Benna, S ;
Hamilton, CA ;
McClure, JD ;
Rogers, PN ;
Berg, GA ;
Ford, I ;
Delles, C ;
Dominiczak, AF .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2006, 26 (01) :218-223
[4]   Gene transfer of endothelial nitric oxide synthase but not Cu/Zn superoxide dismutase restores nitric oxide availability in the SHRSP [J].
Alexander, MY ;
Brosnan, MJ ;
Hamilton, CA ;
Fennell, JP ;
Beattie, EC ;
Jardine, E ;
Heistad, DD ;
Dominiczak, AF .
CARDIOVASCULAR RESEARCH, 2000, 47 (03) :609-617
[5]   Regulation of endothelial nitric oxide synthase by tetrahydrobiopterin in vascular disease [J].
Alp, NJ ;
Channon, KM .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2004, 24 (03) :413-420
[6]   The relationship between plasma levels of oxidized and reduced thiols and early atherosclerosis in healthy adults [J].
Ashfaq, S ;
Abramson, JL ;
Jones, DP ;
Rhodes, SD ;
Weintraub, WS ;
Hooper, WC ;
Vaccarino, V ;
Harrison, DG ;
Quyyumi, AA .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2006, 47 (05) :1005-1011
[7]   Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation [J].
Aviram, M ;
Rosenblat, M ;
Gaitini, D ;
Nitecki, S ;
Hoffman, A ;
Dornfeld, L ;
Volkova, N ;
Presser, D ;
Attias, J ;
Liker, H ;
Hayek, T .
CLINICAL NUTRITION, 2004, 23 (03) :423-433
[8]   N-acetylcysteine potentiates the antihypertensive effect of ACE inhibitors in hypertensive patients [J].
Barrios, V ;
Calderón, A ;
Navarro-Cid, J ;
Lahera, V ;
Ruilope, LM .
BLOOD PRESSURE, 2002, 11 (04) :235-239
[9]   Does vitamin C reduce blood pressure? Results of a large study of people aged 65 or older [J].
Bates, CJ ;
Walmsley, CM ;
Prentice, A ;
Finch, S .
JOURNAL OF HYPERTENSION, 1998, 16 (07) :925-932
[10]   Inhibition of protein kinase Cβ prevents impaired endothelium-dependent vasodilation caused by hyperglycemia in humans [J].
Beckman, JA ;
Goldfine, AB ;
Gordon, MB ;
Garrett, LA ;
Creager, MA .
CIRCULATION RESEARCH, 2002, 90 (01) :107-111