OBJECTIVE: We recently provided evidence for contraction-induced attenuation of reflex sympathetic vasoconstriction in human skeletal muscle microcirculation. We now asked whether contraction-induced modulation of alpha-adrenoceptor mediated vasoconstriction in the human forearm (a) is evident in a large artery supplying the contracting skeletal muscle and (b) implicates a post-junctional site of action. METHODS AND RESULTS: To address these questions in humans, we used phase-contrast magnetic resonance imaging to measure blood flow velocity and cross-sectional area of the brachial artery during brachial-artery infusion of the alpha-adrenoceptor agonist norepinephrine (NE) (1.1 g/min for 5 min) at rest and during mild ipsilateral rhythmic handgrip (20% of maximum). At rest, brachial artery conductance decreased progressively during the entire 5 min period of infusion (baseline to first half to second half of infusion: 0.421 +/- 0.157 to 0.255 +/- 0.187 to 0.012 +/- 0.014 ml/min/mmHg, P < 0.05). When NE was superimposed on handgrip, conductance at first decreased sharply (1.205 +/- 0.127 to 0.330 +/- 0.097 ml/min/mmHg, P < 0.05). However, during the second half of the infusion, conductance did not decrease further but rather returned progressively toward baseline (0.476 +/- 0.199 ml/min/mmHg at the end of the exercise, P < 0.05 vs. NE alone). CONCLUSION: These data provide new evidence in humans that alpha-adrenoceptor mediated vasoconstriction is sensitive to modulation by skeletal muscle contraction. Such modulation is evident at the level of a large conduit artery and it involves a post-junctional mechanism of action.
OBJECTIVE: We recently provided evidence for contraction-induced attenuation of reflex sympathetic vasoconstriction in human skeletal muscle microcirculation. We now asked whether contraction-induced modulation of alpha-adrenoceptor mediated vasoconstriction in the human forearm (a) is evident in a large artery supplying the contracting skeletal muscle and (b) implicates a post-junctional site of action. METHODS AND RESULTS: To address these questions in humans, we used phase-contrast magnetic resonance imaging to measure blood flow velocity and cross-sectional area of the brachial artery during brachial-artery infusion of the alpha-adrenoceptor agonist norepinephrine (NE) (1.1 g/min for 5 min) at rest and during mild ipsilateral rhythmic handgrip (20% of maximum). At rest, brachial artery conductance decreased progressively during the entire 5 min period of infusion (baseline to first half to second half of infusion: 0.421 +/- 0.157 to 0.255 +/- 0.187 to 0.012 +/- 0.014 ml/min/mmHg, P < 0.05). When NE was superimposed on handgrip, conductance at first decreased sharply (1.205 +/- 0.127 to 0.330 +/- 0.097 ml/min/mmHg, P < 0.05). However, during the second half of the infusion, conductance did not decrease further but rather returned progressively toward baseline (0.476 +/- 0.199 ml/min/mmHg at the end of the exercise, P < 0.05 vs. NE alone). CONCLUSION: These data provide new evidence in humans that alpha-adrenoceptor mediated vasoconstriction is sensitive to modulation by skeletal muscle contraction. Such modulation is evident at the level of a large conduit artery and it involves a post-junctional mechanism of action.
Authors: D Walter Wray; Paul J Fadel; David M Keller; Shigehiko Ogoh; Mikael Sander; Peter B Raven; Michael L Smith Journal: J Physiol Date: 2004-07-02 Impact factor: 5.182
Authors: Stephen B Ruble; Zoran Valic; John B Buckwalter; Michael E Tschakovsky; Philip S Clifford Journal: J Physiol Date: 2002-06-01 Impact factor: 5.182