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J Appl Physiol 99: 1622, 2005; doi:10.1152/japplphysiol.00805.2005
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POINT-COUNTERPOINT COMMENTS

Flow-mediated vasodilation partially reflects nitric oxide-mediated endothelial function

Axel Linke, Sandra Erbs, and Rainer Hambrecht

University of Leipzig-Heart Center
Department of Cardiology
Leipzig, Germany
e-mail: linkea{at}medizin.uni-leipzig.de

ABSTRACT

This letter is in response to the Point:Counterpoint series "Flow-mediated dilation does/does not reflect nitric oxide-mediated endothelial function" that appeared in the September issue (vol. 99: 1233–1238, 2005; doi:10.1152/japplphysiol.00601.2005; http://jap.physiology.org/content/vol99/issue3/2005).

To the Editor: In this Point:Counterpoint series, Green and Tschakovsky and Pyke address the issue of whether flow-mediated dilation (FMD) reflects nitric oxide (NO)-mediated endothelial function (1). However, this question is difficult to answer. It has been conclusively shown that FMD of the brachial artery after 5 min of wrist cuff occlusion can be entirely abolished by the NO synthase (NOS) inhibitor NG-monomethyl-L-arginine (L-NMMA), suggesting a complete NO dependency of the process (2). Nevertheless, when the cuff was positioned on the arm above the probe, FMD was found to be 12% and was only reduced to 7.5% by L-NMMA (2). In contrast, Hornig reported a similar vasodilatory response of the radial artery (~12%) independent of whether the occlusion was performed upstream (upper arm) or downstream (wrist) of the site of measurement (3). Interestingly, the increase in radial artery diameter was even more pronounced after longer periods of vessel occlusion before assessment of FMD (~13% after 8 min vs. ~7% after 4 min). The amount of FMD abolished by L-NMMA was ~66% in healthy individuals but ~33% in patients with chronic heart failure (CHF), possibly due to endothelin-mediated vasoconstriction in CHF (1, 3). Therefore, FMD appears to partially reflect NO-mediated endothelial function. The abovementioned data are consistent with the hypothesis that key players other than NO mediating FMD, e.g., prostaglandins and myogenic factors, in different experimental settings depend on 1) the duration of occlusion, 2) the site of measurement in relation to the site of vessel occlusion, and 3) the subjects, in whom the measurements are performed.

REFERENCES

  1. Green D; Tschakovsky ME and Pyke KE. Point/Counterpoint: Flow-mediated dilation does/does not reflect nitric oxide-mediated endothelial function. J Appl Physiol 99: 1233–1238, 2005.[Free Full Text]
  2. Doshi SN, Naka KK, Payne N, Jones CJH, Ashton M, Lewis MJ, and Goodfellow J. Flow-mediated dilatation following wrist and upper arm occlusion in humans: the contribution of nitric oxide. Clin Sci 101: 629–635, 2001.[Medline]
  3. Hornig B, Maier V, and Drexler H. Physical training improves endothelial function in patients with chronic heart failure. Circulation 93: 210–214, 1996.[Abstract/Free Full Text]




This Article
Right arrow Abstract Freely available
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Right arrow Articles by Hambrecht, R.

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