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This Article Full Text Full Text (PDF) All Versions of this Article: 293/4/H2550    most recent 00867.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Wray, D. W. Articles by Richardson, R. S. Search for Related Content PubMed PubMed Citation Articles by Wray, D. W. Articles by Richardson, R. S.

Endothelin-1-mediated vasoconstriction at rest and during dynamic exercise in healthy humans

¹Department of Medicine, University of California San Diego, La Jolla, California; ²Departments of Medicine and Exercise and Sport Science, University of Utah, Salt Lake City, Utah; ³Department of Integrative Physiology, University of Colorado, Boulder, Colorado; ⁴Aviation Medicine and Copenhagen Muscle Research Centre, Department of Cardiology, National Hospital, Copenhagen, Denmark; and ⁵Geriatric Research Education and Clinical Center, Salt Lake City VAMC, Salt Lake City, Utah

Submitted 24 July 2007 ; accepted in final form 9 August 2007

It is now generally accepted that -adrenoreceptor-mediated vasoconstriction is attenuated during exercise, but the efficacy of nonadrenergic vasoconstrictor pathways during exercise remains unclear. Thus, in eight young (23 ± 1 yr), healthy volunteers, we contrasted changes in leg blood flow (ultrasound Doppler) before and during intra-arterial infusion of the ₁-adrenoreceptor agonist phenylephrine (PE) with that of the nonadrenergic endothelin A (ET_A)/ET_B receptor agonist ET-1. Heart rate, arterial blood pressure, common femoral artery diameter, and mean blood velocity were measured at rest and during knee-extensor exercise at 20%, 40%, and 60% of maximal work rate (WR_max). Drug infusion rates were adjusted for blood flow to maintain comparable doses across all subjects and conditions. At rest, PE infusion (8 ng·ml^–1·min^–1) provoked a rapid and significant decrease in leg blood flow (–51 ± 3%) within 2.5 min. Resting ET-1 infusion (40 pg·ml^–1·min^–1) significantly decreased leg blood flow within 5 min, reaching a maximal vasoconstriction (–34 ± 3%) after 25–30 min of continuous infusion. Compared with rest, an exercise intensity-dependent attenuation to PE-mediated vasoconstriction was observed (–18 ± 5%, –7 ± 2%, and –1 ± 3% change in leg blood flow at 20%, 40%, and 60% of WR_max, respectively). Vasoconstriction in response to ET-1 was also blunted in an exercise intensity-dependent manner (–13 ± 3%, –7 ± 4%, and 2 ± 3% change in leg blood flow at 20%, 40%, and 60% of WR_max, respectively). These findings support a significant contribution of ET-1 and -adrenergic receptors in the regulation of skeletal muscle blood flow in the human leg at rest and suggest a similar, intensity-dependent "lysis" of peripheral ET and -adrenergic vasoconstriction during dynamic exercise.

endothelial; -adrenoreceptor; exercise hyperemia; ultrasound Doppler

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