Evidence against oxidative stress as mechanism of endothelial dysfunction in methionine loading model

Angus K. Nightingale, Philip P. James, Jayne Morris-Thurgood, Fraser Harrold, Richard Tong, Simon K. Jackson, John R. Cockcroft, Michael P. Frenneaux*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

19 Citations (Scopus)

Abstract

Endothelial dysfunction reflects reduced nitric oxide (NO) bioavailability due to either reduced production, inactivation of NO, or reduced smooth muscle responsiveness. Oral methionine loading causes acute endothelial dysfunction in healthy subjects and provides a model in which to study mechanisms. Endothelial function was assessed using flow-mediated dilatation (FMD) of the brachial artery in humans. Three markers of oxidative stress were measured ex vivo in venous blood. NO responsiveness was assessed in vascular smooth muscle and platelets. Oral methionine loading induced endothelial dysfunction (FMD decreased from 2.8 ± 0.8 to 0.3 ± 0.3% with methionine and from 2.8 ± 0.8 to 1.3 ± 0.3% with placebo; P < 0.05). No significant changes in measures of plasma oxidative stress or in vascular or platelet sensitivity to submaximal doses of NO donors were detected. These data suggest that oxidative stress is not the mechanism of endothelial dysfunction after oral methionine loading. Furthermore, the preservation of vascular and platelet NO sensitivity makes a signal transduction abnormality unlikely.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume280
Issue number3 49-3
Publication statusPublished - 2001
Externally publishedYes

Keywords

  • Endothelium
  • Homocysteine
  • Oxidative stress
  • Platelet aggregation
  • Signal transduction

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