Inhibition of basal nitric oxide synthesis increases aortic augmentation index and pulse wave velocity in vivo

Ian B. Wilkinson*, Helen MacCallum, John R. Cockcroft, David J. Webb

*Corresponding author for this work

Research output: Contribution to journalArticle

173 Citations (Scopus)

Abstract

Aims: To investigate the role of basal nitric oxide (NO) production in regulating large artery stiffness in vivo. Methods: Incremental doses of the NO synthase inhibitor L-NG-monomethyl arginine (LNMMA: 0.1, 0.3, 1.0 and 3.0 mg kg-1 min-1) or placebo were infused in eight healthy men. Arterial stiffness was assessed noninvasively by pulse wave analysis. Results: Compared with placebo, infusion of LNMMA led to a dose-dependent increase in mean arterial pressure, peripheral vascular resistance, and aortic and systemic arterial stiffness. There was an accompanying reduction in heart rate and cardiac index. The highest dose of LNMMA resulted in an increase of 25% in AIx (95% confidence limits; 12, 38) and of 16 mmHg in mean arterial pressure (9, 23) compared with infusion of saline. Conclusions: These data indicate functional regulation of large artery stiffness in vivo by NO, and may provide new therapeutic strategies for cardiovascular risk reduction.

Original languageEnglish
Pages (from-to)189-192
Number of pages4
JournalBritish Journal of Clinical Pharmacology
Volume53
Issue number2
DOIs
Publication statusPublished - 2002

Keywords

  • Arterial stiffness
  • LNMMA
  • Nitric oxide
  • Pulse wave analysis

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