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Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
08:41

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Endothelial dysfunction and hypertension in aging

Yukihito Higashi1, Yasuki Kihara, Kensuke Noma

  • 1Department of Cardiovascular Regeneration and Medicine, Research Institute for Radiation Biology and Medicine (RIRBM), Hiroshima University, Hiroshima, Japan. yhigashi@hiroshima-u.ac.jp

Hypertension Research : Official Journal of the Japanese Society of Hypertension
|September 14, 2012
PubMed

Insights

Aging exacerbates endothelial dysfunction, a key factor in hypertension development. This review explores how impaired nitric oxide (NO) bioavailability and increased oxidative stress contribute to age-related hypertension and cardiovascular risks.

Area of Science:

  • Cardiovascular Science
  • Gerontology
  • Vascular Biology

Background:

  • Hypertension prevalence significantly increases with age, posing risks for cardiovascular and cerebrovascular complications.
  • Both aging and hypertension independently impair endothelial function, a critical regulator of vascular tone.
  • Endothelial dysfunction, characterized by reduced nitric oxide (NO) bioavailability, contributes to elevated blood pressure.

Purpose of the Study:

  • To review recent findings on the interactions between endothelial function, oxidative stress, and hypertension in the aging process.
  • To elucidate the mechanisms linking aging-induced endothelial dysfunction to increased hypertension risk.
  • To highlight the role of oxidative stress and endothelial cell senescence in age-related vascular changes.

Main Methods:

  • Literature review focusing on recent research in aging, hypertension, endothelial function, and oxidative stress.
  • Analysis of studies investigating the role of nitric oxide (NO) and reactive oxygen species (ROS) in endothelial dysfunction.
  • Examination of evidence linking endothelial cell senescence to age-related vascular pathology.

Main Results:

  • Aging is associated with progressive endothelial dysfunction, partly mediated by increased oxidative stress.
  • An imbalance between reduced NO production and increased superoxide generation promotes endothelial dysfunction.
  • Endothelial cell senescence emerges as a significant factor in age-related endothelial dysfunction and hypertension.

Conclusions:

  • Age-related endothelial dysfunction, driven by oxidative stress and cellular senescence, is a primary mechanism underlying increased hypertension prevalence in the elderly.
  • Maintaining endothelial function and reducing oxidative stress are crucial for mitigating cardiovascular risks associated with aging and hypertension.
  • Further research into the interplay of aging, oxidative stress, and vascular health is warranted to develop effective interventions.

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