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
Language
- eng
Conference Location
- Germany