title: Superiority of endothelin-1 over norepinephrine in exercise-induced alterations of the conduit artery tone of the non-exercised arm in patients with chronic heart failure.
abstract: This study is aimed at examining the relative importance of norepinephrine and endothelin-1 in treadmill exercise-induced changes in brachial arterial tone of the non-exercised arm in patients with chronic heart failure (CHF). Brachial artery diameter and blood flow were measured before and after exercise in eight healthy volunteers and 18 patients with stable chronic heart failure by high-resolution ultrasound. Maximal exercise resulted in brachial artery dilatation in controls (4.42+/-0.39 vs. 4.77+/-0.39 mm; P<0. 0001) in contrast to constriction seen in the patients (5.27+/-0.67 vs. 5.12+/-0.66 mm; P=0.07). Both groups demonstrated a significant increase in blood flow after exercise. The pre-exercise (2.83+/-0.76 vs. 1.69+/-0.15 pmol/l; P=0.0004), post-exercise (4.15+/-1.5 vs. 2. 02+/-0.34 pmol/l; P=0.0004) and the percent increase (47.15+/-32.5 vs. 19.0+/-10.5%; P=0.02) in endothelin-1 levels were significantly greater in patients than in controls. In contrast to endothelin-1, the exercise-induced percent increase in norepinephrine was greater in controls than patients (100.7+/-51.8 vs. 49.8+/-43.4%; P=0.01). The percent change in the diameter of the brachial artery in response to maximal exercise was significantly correlated to pre- (r=0.634; P=0.003) and post-exercise (r=0.467; P=0.05) endothelin-1 levels in patients but not in controls [pre-exercise (r=0.07; P=0. 86), post-exercise (r=0.310; P=0.47)]. The change in the diameter of the brachial artery did not correlate with pre- or post-exercise plasma norepinephrine levels in either group. These findings suggest that endothelin-1 is potentially more important than norepinephrine in contributing exercise-induced brachial artery constriction in patients with chronic heart failure.
authors.affiliation: Divisions of Cardiac Medicine and Biochemistry, National Heart and Lung Institute and Royal Brompton Hospital, London, UK. m.yousufuddin@ic.ac.uk
authors.forename: M
authors.initials: M
authors.lastname: Yousufuddin
authors.forename: W
authors.initials: W
authors.lastname: Shamim
authors.forename: J S
authors.initials: JS
authors.lastname: Chambers
authors.forename: M
authors.initials: M
authors.lastname: Henein
authors.forename: F R
authors.initials: FR
authors.lastname: Amin
authors.forename: S D
authors.initials: SD
authors.lastname: Anker
authors.forename: M
authors.initials: M
authors.lastname: Kemp
authors.forename: J
authors.initials: J
authors.lastname: Hooper
authors.forename: A J
authors.initials: AJ
authors.lastname: Coats
mesh_terms: D001916:Brachial Artery; D019332:Endothelin-1 / Q000097:blood*; D004730:Endothelium, Vascular / Q000378:metabolism; D015444:Exercise / Q000502:physiology*; D006333:Heart Failure / Q000097:blood* / Q000534:rehabilitation; D006439:Hemodynamics; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood*; D012039:Regional Blood Flow; D014661:Vasoconstriction; D014666:Vasomotor System / Q000378:metabolism* / Q000502:physiology
chemical_list: D019332:Endothelin-1; D009638:Norepinephrine