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Updated: Jun 20, 2026

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

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eNOS uncoupling and endothelial dysfunction in aged vessels.

Yang-Ming Yang1, An Huang, Gabor Kaley

  • 1Department of Physiology, New York Medical College, Valhalla, NY 10595, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|September 22, 2009
PubMed
Summary
This summary is machine-generated.

Aging causes endothelial dysfunction by uncoupling endothelial nitric oxide synthase (eNOS). This process involves increased superoxide production and reduced tetrahydrobiopterin (BH4) cofactor, impairing blood vessel function.

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Published on: February 25, 2016

Area of Science:

  • Vascular Biology
  • Aging Research
  • Biochemistry

Background:

  • Endothelial nitric oxide synthase (eNOS) uncoupling contributes to endothelial dysfunction.
  • Aging is associated with reduced nitric oxide release and increased superoxide production in vessels.

Purpose of the Study:

  • To investigate the impact of aging on eNOS uncoupling in mouse mesenteric arteries.
  • To identify molecular mechanisms underlying age-related endothelial dysfunction.

Main Methods:

  • Comparison of eNOS protein expression, monomer/dimer ratio, and superoxide formation in young and aged mice.
  • Measurement of nitrotyrosine levels and tetrahydrobiopterin (BH4) cofactor content.
  • Assessment of GTP cyclohydrolase I and sepiapterin reductase gene expression.
  • Pharmacological intervention with sepiapterin to evaluate vasodilation and eNOS dimer stabilization.

Main Results:

  • Aged mice exhibited increased eNOS monomer/dimer ratio and superoxide production.
  • Nitrotyrosine levels were elevated in aged vessels, indicating increased nitrosylation.
  • Tetrahydrobiopterin (BH4) levels were reduced in aged mesenteric arteries, linked to decreased expression of BH4 biosynthesis enzymes.
  • Sepiapterin treatment improved vasodilation and stabilized eNOS dimers in aged arteries.

Conclusions:

  • Aging promotes eNOS uncoupling and endothelial dysfunction through mechanisms including increased nitrosylation and reduced BH4 bioavailability.
  • Decreased expression of BH4 biosynthesis enzymes contributes to diminished BH4 levels in aged vessels.
  • Restoring BH4 levels via sepiapterin can ameliorate age-related endothelial dysfunction.