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This Article Full Text Full Text (PDF) All Versions of this Article: 93/4/503    most recent expphysiol.2007.041129v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Nier, B. A. Articles by Weinberg, P. D. Search for Related Content PubMed PubMed Citation Articles by Nier, B. A. Articles by Weinberg, P. D.

¹ Department of Bioengineering² The National Heart and Lung Institute, Imperial College, London, UK³ William Harvey Research Institute, Queen Mary's School of Medicine and Dentistry, London, UK

The height of the dicrotic notch between the systolic and diastolic peaks of the peripheral pulse wave, expressed as a fraction of the overall amplitude of the wave, is sensitive to nitric oxide (NO) bioactivity. This phenomenon might form the basis of a simple, non-invasive method for determining endothelial function in vivo. We assessed whether the phenomenon is specific to the NO pathway or whether other vasoactive agents have similar effects. The relative height of the dicrotic notch (RHDN) was determined by photoplethysmography in the rabbit ear. It was dose-dependently decreased by acetylcholine, a stimulator of endothelial NO synthesis, and increased by N^G-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthesis. There was no effect on RHDN of the -adrenergic blocker phentolamine or the β-adrenergic blocker propranolol. The cyclo-oxygenase inhibitor indomethacin dose-dependently decreased RHDN but this effect was blocked by L-NAME, suggesting it was mediated by cross-talk with the NO pathway. Changes in RHDN appeared to be independent of heart rate and of the delay between the systolic peak and the notch, but were associated with changes in the slope of the dicrotic limb. Both L-NAME and phentolamine produced multiple diastolic peaks, indicative of wave reflections in the vasculature. These data support the view that changes in RHDN are specific to the NO pathway and provide additional information about the mechanisms involved.

(Received 18 October 2007; accepted after revision 22 January 2008; first published online 25 January 2008)
Corresponding author P. D. Weinberg: Department of Bioengineering, Imperial College, London SW7 2AZ, UK. Email: p.weinberg{at}imperial.ac.uk