Endothelial dysfunction in hypercholesterolemia is corrected by L-arginine.

J. P. Cooke, J. Dzau, A. Creager

Research output: Contribution to journalArticle

31 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)173-181
Number of pages9
JournalBasic research in cardiology
Volume86 Suppl 2
DOIs
StatePublished - 1991

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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