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J Appl Physiol 99: 1627, 2005; doi:10.1152/japplphysiol.00387.2005
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POINT-COUNTERPOINT COMMENTS

FMD vs. pharmacological approaches for endothelial function

Hirofumi Tanaka

Department of Kinesiology
University of Wisconsin-Madison
Madison, Wisconsin
e-mail: tanaka1{at}wisc.edu

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: As an investigator who has used the flow-mediated dilatation (FMD) technique, I read the debate (2) with great interest. Several years ago, we asked a similar question by comparing two typical approaches to study endothelium-dependent vasodilation (brachial artery FMD and intrabrachial infusion of acetylcholine). Surprisingly, we found that these two common experimental approaches do not correlate (1). Because the pharmacological approach was considered as a "gold standard" for the measurements of endothelial function, these results could be taken as the evidence against the FMD method. However, when the acetylcholine responses were inhibited by the nitric oxide inhibitor NG-monomethyl-L-arginine (L-NMMA), only about 30–40% of the responses were blocked (4). In contrast, FMD is completely abolished by the infusion of L-NMMA (3). Thus FMD appears to reflect nitric oxide-mediated endothelial function, at least more than the pharmacological approach, and is a promising noninvasive technique for the assessment of endothelial function. However, if this is going to be a useful clinical and research technique, several issues regarding the methodology (e.g., location and duration of occlusion, timing of peak hyperemia, widely different normative values between studies) and interpretation/confounders (e.g., differences in arterial inflow, inverse relation with baseline diameter, influences of sympathetic tone) should be properly addressed.

REFERENCES

  1. Eskurza I, Seals DR, DeSouza CA, and Tanaka H. Pharmacological vs H flow-mediated assessments of peripheral vascular endothelial vasodilatory function in humans. Am J Cardiol 88: 47–49, 2001.
  2. Green G; 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]
  3. Joannides R, Richard V, Haefeli WE, Benoist A, Linder L, Luscher TF, and Thuillez C. Role of nitric oxide in the regulation of the mechanical properties of peripheral conduit arteries in humans. Hypertension 30: 1465–1470, 1997.[Abstract/Free Full Text]
  4. Newby DE, Boon NA, and Webb DJ. Comparison of forearm vasodilatation to substance P and acetylcholine: contribution of nitric oxide. Clin Sci (Colch) 92: 133–138, 1997.[Medline]




This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
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PubMed
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