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[Oxidative stress, reactive oxygen species].

Yukihito Higashi1, Masao Yoshizumi

  • 1Department of Cardiovascular Physiology and Medicine, Graduate School of Biomedical Sciences, Hiroshima University.

Nihon Rinsho. Japanese Journal of Clinical Medicine
|January 24, 2004
PubMed
Summary

Hypertension causes organ damage through oxidative stress, which impairs endothelial function. This review details how oxidative stress contributes to cardiovascular and cerebrovascular issues in hypertensive patients.

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Area of Science:

  • Cardiovascular Science
  • Oxidative Stress Research
  • Endothelial Function Studies

Context:

  • Hypertension is a major risk factor for cardiovascular and cerebrovascular diseases.
  • Endothelial dysfunction is an early event in atherosclerosis development.
  • Oxidative stress plays a critical role in the pathophysiology of hypertension.

Purpose:

  • To review the role of oxidative stress in hypertensive organ damage.
  • To explain the mechanisms by which oxidative stress affects vascular health.
  • To highlight the link between oxidative stress and atherosclerosis in hypertension.

Summary:

  • Oxidative stress, driven by reactive oxygen species (ROS), disrupts the balance between superoxide and nitric oxide (NO), leading to endothelial dysfunction.

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  • Angiotensin II and mechanical stress activate NADH/NADPH oxidase in hypertension, increasing ROS production.
  • Oxidative stress contributes to vascular growth, inflammation, and impaired endothelium-dependent relaxation in hypertension.

    • Impact:

    • Understanding the role of oxidative stress is crucial for developing targeted therapies for hypertensive organ damage.
    • This review provides insights into the molecular mechanisms underlying hypertension-related complications.
    • Elucidating the link between oxidative stress and endothelial dysfunction can inform strategies to prevent cardiovascular and cerebrovascular events.