Oxidative stress and human hypertension: vascular mechanisms, biomarkers, and novel therapies.
Hypertension is a major cardiovascular risk factor. Of the many processes involved in the pathophysiology of hypertension, vascular damage due to oxidative stress (excess bioavailability of reactive oxygen species [ROS]) is particularly important. Physiologically, ROS regulate vascular function through redox-sensitive signalling pathways. In hypertension, oxidative stress promotes endothelial dysfunction, vascular remodelling, and inflammation, leading to vascular damage. Vascular ROS are derived primarily by nicotinamide adenine dinucleotide phosphate oxidases, which are prime targets for therapeutic development. Although experimental evidence indicates a causative role for oxidative stress in hypertension, human data are less convincing. This might relate, in part, to suboptimal methods to accurately assess the redox state. Herein we review current knowledge on oxidative stress in vascular pathobiology and implications in human hypertension. We also discuss biomarkers to assess the redox state in the clinic, highlight novel strategies to inhibit ROS production, and summarize how lifestyle modifications promote vascular health by reducing oxidative stress.
Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland.
Augusto C
AC
Montezano
Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland.
Maria
M
Dulak-Lis
Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland.
Sofia
S
Tsiropoulou
Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland.
Adam
A
Harvey
Departmento de Farmacología, Universidad Autónoma de Madrid (UAM), Instituto de Investigación Hospital Universitario La Paz (IdiPAZ), Madrid, Spain.
Ana M
AM
Briones
Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, Scotland. Electronic address: Rhian.Touyz@glasgow.ac.uk.
Rhian M
RM
Touyz
D000493:Allopurinol / Q000627:therapeutic use; D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D002320:Cardiovascular Physiological Phenomena / Q000187:drug effects; D005260:Female; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy*; D008019:Life Style; D008297:Male; D019255:NADPH Oxidases / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D011379:Prognosis; D017382:Reactive Oxygen Species / Q000378:metabolism*; D018570:Risk Assessment; D012720:Severity of Illness Index; D016896:Treatment Outcome; D014969:Xanthine Oxidase / Q000037:antagonists & inhibitors
D000959:Antihypertensive Agents; D000975:Antioxidants; D015415:Biomarkers; D017382:Reactive Oxygen Species; D000493:Allopurinol; D014969:Xanthine Oxidase; D019255:NADPH Oxidases