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Related Experiment Videos

Endothelial dysfunction in hypercholesterolemia is corrected by L-arginine.

J P Cooke1, J Dzau, A Creager

  • 1Division of Cardiovascular Medicine, Falk Cardiovascular Research Center, Stanford University School of Medicine, California.

Basic Research in Cardiology
|January 1, 1991
PubMed
Summary

High cholesterol impairs blood vessel function by reducing nitric oxide. Supplementing with L-arginine, the precursor to nitric oxide, can reverse this endothelial dysfunction in hypercholesterolemia.

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Area of Science:

  • Cardiovascular Science
  • Endothelial Function
  • Metabolic Disorders

Background:

  • Hypercholesterolemia impairs endothelium-dependent vasorelaxation and enhances vasoconstrictor responses.
  • These vascular abnormalities are primarily linked to reduced release of endothelium-derived relaxing factor (EDRF).
  • EDRF is identified as nitric oxide (NO), synthesized from L-arginine metabolism.

Purpose of the Study:

  • To investigate if supplementing L-arginine can correct vascular dysfunction in hypercholesterolemia.
  • To test the hypothesis that impaired L-arginine availability or metabolism contributes to endothelial dysfunction in high cholesterol states.

Main Methods:

  • Studies conducted on hypercholesterolemic animal models.
  • Assessment of conduit and resistance vessel function.

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  • Exposure of vessels to exogenous L-arginine.

    • Main Results:

    • Hypercholesterolemic animals exhibited endothelial dysfunction.
    • Exposure to high concentrations of L-arginine reversed the observed endothelial dysfunction.
    • Vascular responses in hypercholesterolemic vessels were restored towards normal.

    Conclusions:

    • Hypercholesterolemia-induced endothelial dysfunction is reversible.
    • The findings suggest a critical role for L-arginine availability or metabolism in hypercholesterolemia.
    • L-arginine supplementation may represent a therapeutic strategy for managing vascular complications of high cholesterol.