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Relationship between hypercholesterolaemia, endothelial dysfunction and hypertension.

H Hayakawa1, L Raij

  • 1Department of Medicine, Veterans Affairs Medical Center and University of Minnesota Medical School, Minneapolis 55417, USA.

Journal of Hypertension
|July 14, 1999
PubMed
Summary
This summary is machine-generated.

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A diet high in cholesterol and low in vitamin E and selenium impairs nitric oxide (NO) bioavailability, leading to endothelial dysfunction. This dysfunction increases salt sensitivity without causing hypertension, suggesting lipid oxidation impacts NO bioactivity.

Area of Science:

  • Cardiovascular Physiology
  • Nutritional Science
  • Endothelial Function

Background:

  • Hypercholesterolemia and nutrient deficiencies (vitamin E, selenium) induce oxidative stress.
  • Previous studies in rats showed this diet causes hypercholesterolemia and increased lipid oxidation.

Purpose of the Study:

  • To investigate if this diet impairs endothelium-dependent relaxation mediated by nitric oxide (NO) in mesenteric and renal vessels.
  • To determine the mechanisms of impairment: decreased NO synthase activity, increased NO inactivation, or increased constricting factors.
  • To assess if endothelial dysfunction increases hypertension sensitivity to high salt intake.

Main Methods:

  • Male Dahl salt-sensitive rats were fed standard, high cholesterol, or high cholesterol with antioxidant deficiency diets.

Related Experiment Videos

  • Endothelium-dependent relaxation to acetylcholine was assessed in aortas, mesenteric arteries, and kidneys.
  • Vascular responses to endothelin-1 and effects of specific receptor antagonists were evaluated.
  • Sensitivity to high salt diet was tested in separate groups.

    • Main Results:

    • Endothelium-dependent relaxation was significantly impaired in high cholesterol-deficient rats.
    • Impairment was not due to reduced endothelial NO synthase activity.
    • Thromboxane A2/prostaglandin H2 receptor antagonism improved relaxation in mesenteric vessels only.
    • Kidneys from deficient rats showed impaired NO-mediated relaxation to endothelin-1.
    • Despite dysfunction, these rats did not develop hypertension but showed increased sensitivity to high salt.

    Conclusions:

    • Lipid oxidation products can reduce NO bioactivity without altering NO synthase activity.
    • Mechanisms of endothelial dysfunction vary across different blood vessels.
    • Reduced NO bioavailability enhances salt sensitivity but doesn't invariably lead to hypertension.