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J Appl Physiol 99: 1621, 2005; doi:10.1152/japplphysiol.00817.2005
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POINT-COUNTERPOINT COMMENTS

Flow-mediated dilation does/does not reflect nitric oxide-mediated endothelial function

Clare E. Austin

Department of Medicine
University of Manchester
Manchester, United Kingdom
e-mail: clare.austin{at}man.ac.uk

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: Responses of small arteries to flow have been shown to be dependent, partially dependent, and indeed independent of nitric oxide (NO; see September Point-Counterpoint, Ref. 1). As such, although NO may clearly modulate flow-mediated dilatory responses, the response does not purely reflect NO-mediated endothelial function. Why then do we see these differences? Although variations in species and arterial size may contribute, the complexity of the endothelial factor system itself is likely to underpin these observations. It is well known that there may be cross-talk between the different endothelial factor synthesis pathways such that inhibition or ablation of one may be compensated for by increased activity of another. For example, in endothelial NO synthase knockout (KO) mice, flow-mediated dilation is maintained by EDHF, whereas in wild-type animals it is mediated by NO (2). As such, the contribution of NO to the response may vary with physiological and pathophysiological conditions and indeed with experimental modulation of different endothelial factor pathways (e.g., use of different inhibitors/inhibitor combinations or KO animals). A novel suggestion is that the involvement of NO may also vary with the duration of the flow stimulus; inhibition of NOS inhibited vasodilation to sustained flow but was without effect on the immediate response to increased flow (3). Thus NO appears to play a varied role in mediating flow-induced dilatory responses. The involvement of other factors in certain conditions, however, means that flow-mediated dilation does not necessarily reflect NO-mediated endothelial function.

REFERENCES

  1. 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]
  2. Huang, Sun AD, Carroll MA, Jiang H, Smith CJ, Connetta JA, Falk JR, Shesely EG, Koller A, and Kaley G. EDHF mediates flow-induced dilation in skeletal muscle arterioles of female eNOS-KO mice. Am J Physiol Heart Circ Physiol 280: H2462–H2469, 2001.[Abstract/Free Full Text]
  3. Shipley RD, Kim SJ, and Muller-Delp JM. Time course of flow-induced vasodilation in skeletal muscle: contributions of dilator and constrictor mechanisms. Am J Physiol Heart Circ Physiol 288: H1499–H1507, 2005.[Abstract/Free Full Text]




This Article
Right arrow Abstract Freely available
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