title: Flow-mediated dilation of the radial artery is offset by flow-induced reduction in transmural pressure.
abstract: Flow-mediated dilation of the brachial or radial artery in response to transient hyperaemic flow, the most widely used test of endothelial function, is only manifest after flow decays back to baseline. We examined whether this dissociation of flow and diameter might be explained by a reduction in transmural pressure generated by high flow. Studies were performed in healthy subjects 20 to 55 years of age. Flow-mediated dilation was measured in the radial artery using a standard protocol and after flow interruption at peak hyperemia during brachial artery infusion of saline and the NO synthase inhibitor N(G)-monomethyl-L-arginine (8 μmol/min). Flow interruption 20 seconds after cuff release (during high flow but no dilatation) produced an immediate increase in radial artery diameter of 5.36±2.12%, inhibited by N(G)-monomethyl-L-arginine to 1.09±0.67% (n=8; P<0.001). Mean intra-arterial radial blood pressure and, hence, transmural pressure fell after cuff release by a mean of 26±1.8 mm Hg (n=6; P<0.0001) at the time of peak hyperemic flow. Modulation of transmural pressure within the brachial artery by cuff inflation around the artery demonstrated that this fall is sufficient to reduce arterial diameter by an amount similar to flow-mediated dilation. These results suggest that flow-dependent, NO-dependent dilation is offset by a flow-induced fall in local arterial pressure and, hence, in transmural pressure. Shear related NO release is likely to play a greater role in the short-term regulation of arterial tone than that suggested by flow-mediated dilation.
authors.affiliation: King's College London, British Heart Foundation Centre, London, United Kingdom.
authors.forename: Benyu
authors.initials: B
authors.lastname: Jiang
authors.forename: Mike
authors.initials: M
authors.lastname: Seddon
authors.forename: Henry
authors.initials: H
authors.lastname: Fok
authors.forename: Ann
authors.initials: A
authors.lastname: Donald
authors.forename: Phil
authors.initials: P
authors.lastname: Chowienczyk
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000328:Adult; D000704:Analysis of Variance; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D001916:Brachial Artery / Q000187:drug effects / Q000502:physiology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D010646:Phentolamine / Q000494:pharmacology; D017534:Radial Artery / Q000187:drug effects / Q000502:physiology*; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D055815:Young Adult; D019323:omega-N-Methylarginine / Q000494:pharmacology
chemical_list: D000317:Adrenergic alpha-Antagonists; D004791:Enzyme Inhibitors; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D010646:Phentolamine