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

Research output: Contribution to journalArticle

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
Original languageEnglish
Pages (from-to)H1334-H1339
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume280
Issue number3
DOIs
Publication statusPublished - Mar 2001

Keywords

  • Adolescent
  • Adult
  • Aged
  • Brachial Artery
  • Cross-Over Studies
  • Endothelium, Vascular
  • Homocysteine
  • Humans
  • Lipid Peroxidation
  • Male
  • Methionine
  • Middle Aged
  • Nitrates
  • Oxidative Stress
  • Platelet Aggregation
  • Prospective Studies
  • Signal Transduction
  • Thiobarbituric Acid Reactive Substances

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