Key result
Impaired flow-mediated dilation of the brachial artery may result from decreased flow velocity and shear stress during reactive hyperemia rather than impaired nitric oxide release.
This editorial highlights that impaired flow-mediated dilation may stem from reduced shear stress stimulus due to microvascular dysfunction rather than primary endothelial NO release impairment.
In this edition of Hypertension, the Framingham HeartStudy group reports on the relationship between diastolicshear stress and brachial artery flow mediated dilation (FMD) in 2045 participants of the Framingham Offspring group.1 Clinical correlates and heritability of FMD in the participants have been published previously.2 The new report1 challenges conventional concepts on endothelial function and on modification of endothelial function by risk factors of cardiovascular disease. The authors conclude that when present, impaired FMD of the brachial artery may be due not to impaired release of NO from the vascular endothelium, but from a lesser stimulus to NO release as a consequence of decreased flow velocity (and shear stress) during reactive hyperemia caused by impaired microvascular response. Are there fewer peripheral vessels capable of responding to local ischemia? The method used by the authors differed from those
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O’Rourke et al. (2004) reported an editorial. Diastolic shear stress was evaluated on Brachial artery flow-mediated dilation (FMD). Impaired flow-mediated dilation of the brachial artery may result from decreased flow velocity and shear stress during reactive hyperemia rather than impaired nitric oxide release.
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