Endothelial dysfunction in hypercholesterolemia is corrected by L-arginine.

Journal Article (Journal Article)

Hypercholesterolemia attenuates endothelium-dependent vasorelaxation and augments the responses to vasoconstrictor agents. Both effects are largely due to a reduction in the release of endothelium-derived relaxing factor. Since endothelium-derived relaxing factor is now known to be nitric oxide derived from the metabolism of L-arginine, we hypothesized that the abnormal vascular response in hypercholesterolemia could be corrected by supplying the precursor to EDRF, L-arginine. In a series of studies, we have found that conduit and resistance vessels of hypercholesterolemic animals demonstrate endothelial dysfunction which is reversed after exposure to high concentrations of exogenous L-arginine. The experiments suggest that hypercholesterolemia induces a reversible dysfunction of arginine availability or metabolism.

Full Text

Duke Authors

Cited Authors

  • Cooke, JP; Dzau, J; Creager, A

Published Date

  • 1991

Published In

Volume / Issue

  • 86 Suppl 2 /

Start / End Page

  • 173 - 181

PubMed ID

  • 1953609

International Standard Serial Number (ISSN)

  • 0300-8428

Digital Object Identifier (DOI)

  • 10.1007/978-3-642-72461-9_17


  • eng

Conference Location

  • Germany