TY - JOUR
T1 - Exercise-induced attenuation of alpha-adrenoceptor mediated vastconstriction in humans
T2 - Evidence from phase-contrast MRI
AU - Hansen, Jim
AU - Sayad, Dany
AU - Thomas, Gail D.
AU - Clarke, Geoffrey D.
AU - Peshock, Ronald M.
AU - Victor, Ronald G.
N1 - Funding Information:
Dr. Hansen is the recipient of a Fogarty International Research Fellowship (NIH-1-F05-TW04949-01) and were supported by grants from the Danish Heart Foundation, the Simonsen and Weel Foundation and the Danish Research Academy. Dr. Thomas was supported by a National Institutes of Health training grant (T32-HL-07360) and a Muscular Dystrophy Association Postdoctoral Fellowship. Dr. Victor is an Established Investigator of the American Heart Association. This research was supported by a grant to Dr. Victor from the National Institutes of Health (PO1-HL-06296).
PY - 1999/1/1
Y1 - 1999/1/1
N2 - Objective: We recently provided evidence for contraction-induced attenuation of reflex sympathetic vastconstriction 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 vastconstriction 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.
AB - Objective: We recently provided evidence for contraction-induced attenuation of reflex sympathetic vastconstriction 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 vastconstriction 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.
UR - http://www.scopus.com/inward/record.url?scp=0032927540&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032927540&partnerID=8YFLogxK
U2 - 10.1016/S0008-6363(98)00226-0
DO - 10.1016/S0008-6363(98)00226-0
M3 - Article
C2 - 10325969
AN - SCOPUS:0032927540
SN - 0008-6363
VL - 41
SP - 220
EP - 228
JO - Cardiovascular Research
JF - Cardiovascular Research
IS - 1
ER -