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-adrenergic-receptor responsiveness in
skeletal muscle vasculature
Departments of Anesthesiology and Physiology, Medical College of Wisconsin and Veterans Affairs Medical Center, Milwaukee, Wisconsin 53295
Attenuation of sympathetic vasoconstriction
(sympatholysis) in working muscles during dynamic exercise is
controversial. A potential mechanism is a reduction in
-adrenergic-receptor responsiveness. The purpose of this study was
to examine 1- and 2-adrenergic-receptor-mediated vasoconstriction in
resting and exercising skeletal muscle using intra-arterial infusions
of selective agonists. Thirteen mongrel dogs were instrumented
chronically with flow probes on the external iliac arteries of both
hindlimbs and a catheter in one femoral artery. The selective
1-adrenergic agonist (phenylephrine) or the selective
2-adrenergic agonist (clonidine) was infused as a bolus
into the femoral artery catheter at rest and during mild and heavy
exercise. Intra-arterial infusions of phenylephrine elicited reductions
in vascular conductance of 76 ± 4, 71 ± 5, and 31 ± 2% at rest, 3 miles/h, and 6 miles/h and 10% grade, respectively.
Intra-arterial clonidine reduced vascular conductance by 81 ± 5, 49 ± 4, and 14 ± 2%, respectively. The response to
intra-arterial infusion of clonidine was unaffected by surgical
sympathetic denervation. Agonist infusion did not affect either
systemic blood pressure, heart rate, or blood flow in the contralateral
iliac artery. 1-Adrenergic-receptor responsiveness was
attenuated during heavy exercise. In contrast,
2-adrenergic-receptor responsiveness was attenuated even
at a mild exercise intensity. These results suggest that the mechanism
of exercise sympatholysis may involve reductions in postsynaptic
-adrenergic-receptor responsiveness.
blood flow; sympatholysis; autonomic nervous system; dogs; vasoconstriction
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