Acute hyperhomocysteinemia decreases NO bioavailability in healthy adults

Silvana C. Romerio, Lilly Linder, Jürg Nyfeler, Markus Wenk, Piotr Litynsky, Reto Asmis, Walter E. Haefeli

Research output: Contribution to journalArticlepeer-review

33 Scopus citations

Abstract

Hyperhomocysteinemia is associated with decreased vascular reactivity and increased cardiovascular morbidity. Oxidative stress and reduced NO bioavailability have been proposed as a mechanism for the adverse effects of chronically elevated plasma homocysteine levels. Recent studies suggest that acute elevations of plasma homocysteine may also impair endothelial function and vasodilation, however, the mechanism is not clear. In the present study, we investigated whether moderate hyperhomocysteinemia after methionine loading decreases NO bioavailability, increases oxidative stress, and impairs receptor-mediated NO-dependent venodilation in healthy adults. After oral methionine loading (0.1 g/kg), mean homocysteine concentrations increased 3.2-fold, from 6.9 ± 0.5 to 27.8 ± 1.9 μmol/l (n = 16), whereas plasma NOx concentrations, an indicator of NO release, were decreased by 12% compared to placebo treatment (P = 0.005). Vitamin E levels in freshly isolated low density lipoprotein (LDL), a sensitive marker of LDL oxidation, and LDL lipid (hydro)peroxide levels were unchanged after methionine loading. Endothelium-dependent venodilation induced by bradykinin was reduced by 18% during hyperhomocysteinemia (P = 0.06). Taken together our data suggest that the reduced NO bioavailability was likely due to decreased NO synthesis and release rather than to NO destruction by oxidative stress.

Original languageEnglish (US)
Pages (from-to)337-344
Number of pages8
JournalAtherosclerosis
Volume176
Issue number2
DOIs
StatePublished - Oct 2004

Keywords

  • Glutathione peroxidase
  • Hyperhomocysteinemia
  • Lipid peroxidation
  • Nitric oxide
  • Venodilation
  • Vitamin E

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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