Oxidative stress : a unifying paradigm in hypertension

Touyz, Rhian M. and Rios, Francisco J. and Alves-Lopes, Rhéure and Neves, Karla B. and Camargo, Livia L. and Montezano, Augusto C. (2020) Oxidative stress : a unifying paradigm in hypertension. Canadian Journal of Cardiology, 36 (5). pp. 659-670. ISSN 0828-282X (https://doi.org/10.1016/j.cjca.2020.02.081)

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Abstract

The etiology of hypertension involves complex interactions among genetic, environmental, and pathophysiologic factors that influence many regulatory systems. Hypertension is characteristically associated with vascular dysfunction, cardiovascular remodelling, renal dysfunction, and stimulation of the sympathetic nervous system. Emerging evidence indicates that the immune system is also important and that activated immune cells migrate and accumulate in tissues promoting inflammation, fibrosis, and target-organ damage. Common to these processes is oxidative stress, defined as an imbalance between oxidants and antioxidants in favour of the oxidants that leads to a disruption of oxidation-reduction (redox) signalling and control and molecular damage. Physiologically, reactive oxygen species (ROS) act as signalling molecules and influence cell function through highly regulated redox-sensitive signal transduction. In hypertension, oxidative stress promotes posttranslational modification (oxidation and phosphorylation) of proteins and aberrant signalling with consequent cell and tissue damage. Many enzymatic systems generate ROS, but NADPH oxidases (Nox) are the major sources in cells of the heart, vessels, kidneys, and immune system. Expression and activity of Nox are increased in hypertension and are the major systems responsible for oxidative stress in cardiovascular disease. Here we provide a unifying concept where oxidative stress is a common mediator underlying pathophysiologic processes in hypertension. We focus on some novel concepts whereby ROS influence vascular function, aldosterone/mineralocorticoid actions, and immunoinflammation, all important processes contributing to the development of hypertension.

ORCID iDs

Touyz, Rhian M., Rios, Francisco J., Alves-Lopes, Rhéure, Neves, Karla B. ORCID logoORCID: https://orcid.org/0000-0001-5158-9263, Camargo, Livia L. and Montezano, Augusto C.;
  • Item type:Article
    ID code:82879
    Dates:
    Date
    Event
    31 May 2020
    Published
    24 February 2020
    Published Online
    19 February 2020
    Accepted
    Notes:Funding Information: The authors are funded by grants from the British Heart Foundation (BHF; RE/18/6/34217), R.M.T. is supported through a BHF Chair award (CH/12/29762), and A.C.M. is supported through a Walton Foundation fellowship, University of Glasgow . Publisher Copyright: © 2020 The Authors
    Subjects:Medicine > Therapeutics. Pharmacology
    Department:Faculty of Science > Strathclyde Institute of Pharmacy and Biomedical Sciences
    Depositing user: Pure Administrator
    Date deposited:21 Oct 2022 13:14
    Last modified:14 Nov 2024 11:19
    URI:https://strathprints.strath.ac.uk/id/eprint/82879
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