Received October 18, 2007
Revised November 19, 2007
Accepted after revision January 22, 2008
Evidence for a specific influence of the nitrergic pathway on the peripheral pulse waveform in rabbits
Bettina A Nier 1,
Louise S Harrington 1,
Martin J Carrier 2,
Peter D Weinberg 1*
1 Imperial College London
2 Queen Mary University of London
* To whom correspondence should be addressed. E-mail: p.weinberg{at}imperial.ac.uk.
 |
Abstract |
|---|
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 NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthesis. There was no effect on RHDN of the á-adrenergic blocker phentolamine or the â-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 crosstalk with the NO pathway. Changes in RHDN appeared to be independent of heart rate and the delay between the systolic peak and the notch, but were associated with changes in the slope of the dicrotic limb. L-NAME and phentolamine both 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.
Key Words:
Endothelium, Nitric oxide, Plethysmography
