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Evaluation of Vascular Control Mechanisms Utilizing Video Microscopy of Isolated Resistance Arteries of Rats
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L-arginine normalizes endothelial function in cerebral vessels from hypercholesterolemic rabbits.

E Rossitch1, E Alexander, P M Black

  • 1Division of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School.

The Journal of Clinical Investigation
|April 1, 1991
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High cholesterol impairs blood vessel function, causing abnormal constriction and relaxation. Supplementing with L-arginine, the precursor of endothelium-derived relaxing factor, reversed these effects in hypercholesterolemic rabbits, restoring normal vascular reactivity.

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Area of Science:

  • Cardiovascular Biology
  • Endothelial Function Research
  • Pharmacology

Background:

  • Hypercholesterolemia is associated with endothelial dysfunction, impacting vascular tone.
  • Endothelium-derived relaxing factor (EDRF) plays a crucial role in maintaining vascular homeostasis.
  • Impaired EDRF production or activity contributes to the pathophysiology of hypercholesterolemia.

Purpose of the Study:

  • To investigate the effect of L-arginine supplementation on vascular reactivity in hypercholesterolemic rabbits.
  • To determine if L-arginine can restore normal endothelial function in vessels affected by high cholesterol.
  • To assess the stereospecificity of L-arginine's effects on vascular tone.

Main Methods:

  • Basilar arteries were isolated from rabbits fed a normal or cholesterol-supplemented diet for 10 weeks.
  • Vascular reactivity was assessed using videomicroscopy under controlled perfusion pressure.
  • Changes in vessel diameter were measured in response to vasoconstrictors (KCl, endothelin, 5-HT) and vasodilators (acetylcholine, verapamil).
  • In vitro administration of L-arginine or D-arginine was performed to evaluate their effects.

Main Results:

  • Hypercholesterolemic vessels showed enhanced vasoconstriction to KCl, endothelin, and 5-HT.
  • Vasodilation to acetylcholine was significantly impaired in hypercholesterolemic vessels.
  • In vitro L-arginine treatment normalized vasodilation to acetylcholine and vasoconstriction to endothelin, 5-HT, and KCl.
  • D-arginine had no significant effect, indicating stereospecificity.

Conclusions:

  • Hypercholesterolemia induces reversible endothelial dysfunction, characterized by impaired relaxation and increased sensitivity to vasoconstrictors.
  • In vitro L-arginine administration effectively restored normal vascular reactivity in isolated vessels from hypercholesterolemic rabbits.
  • Supplying L-arginine, the precursor of EDRF, represents a potential therapeutic strategy for correcting hypercholesterolemia-induced endothelial dysfunction.