Impairment of endothelium-dependent arterial relaxation by lysolecithin in modified low-density lipoproteins

Nature. 1990 Mar 8;344(6262):160-2. doi: 10.1038/344160a0.


Atherosclerosis in animals and humans is associated with an unresponsiveness of arteries and arterioles to endothelium-dependent vasodilators--agents acting on smooth muscle indirectly by stimulating the release from endothelial cells of a vasodilator principle (endothelium-derived relaxing factor). Altered vasomotor regulation in atherosclerosis could partly reflect an injurious action of abnormal lipoproteins on endothelium. Recently, 'cell-modified' or 'oxidized' low-density lipoprotein (EC-LDL) has received increasing attention because of its potential cytotoxic and atherogenic properties. We report here that arteries exposed to EC-LDL in vitro show an endothelium-dependent vasoregulatory impairment closely resembling that of atherosclerotic arteries. Our results indicate that transfer of lysolecithin from EC-LDL to endothelial membranes produces a selective unresponsiveness to receptor-regulated endothelium-dependent vasodilators.

MeSH terms

  • Acetylcholine / pharmacology
  • Animals
  • Aorta / drug effects
  • Aorta / physiology*
  • Calcimycin / pharmacology
  • Cells, Cultured
  • Endothelium, Vascular / physiology*
  • In Vitro Techniques
  • Kinetics
  • Lipoproteins, LDL / pharmacology*
  • Lysophosphatidylcholines / pharmacology*
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / physiology*
  • Nitroglycerin / pharmacology
  • Oxidation-Reduction
  • Phenylephrine / pharmacology
  • Rabbits
  • Vasodilation / drug effects*


  • Lipoproteins, LDL
  • Lysophosphatidylcholines
  • Phenylephrine
  • Calcimycin
  • Nitroglycerin
  • Acetylcholine