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1 Anesthesiology and Physiology, Medical College of Wisconsin/VA Medical Center, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: jbuckwal{at}mcw.edu.
The production of nitric oxide is the putative mechanism for the attenuation of sympathetic vasoconstriction (sympatholysis) in working muscles during exercise. We hypothesized that nitric oxide synthase blockade would eliminate the reduction in 
adrenergic receptor responsiveness in exercising skeletal muscle. Ten mongrel dogs were instrumented chronically with flowprobes 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. Before nitric oxide synthase inhibition with L-NAME, intraarterial infusions of phenylephrine elicited reductions in vascular conductance of -91±3, -80±5, and -75±6% (mean±SEM) at rest, 3 miles/h, and 6 miles/h 10% grade, respectively. Intraarterial clonidine reduced vascular conductance by -65±6, -39±4, and -30±3%. After L-NAME, intraarterial infusions of phenylephrine elicited reductions in vascular conductance of -85±5, -85±5, and -84±5%, while clonidine reduced vascular conductance by -67±5, -45±3, and -35±3%, at rest, 3 miles/h, and 6 miles/h 10% grade. Alpha1 adrenergic receptor responsiveness was attenuated during heavy exercise. In contrast, 2 adrenergic receptor responsiveness was attenuated even at a mild exercise intensity. Whereas the inhibition of nitric oxide production eliminated the exercise induced attenuation of 1 adrenergic receptor responsiveness, the attenuation of 2 adrenergic receptor responsiveness was unaffected. These results suggest that the mechanism of exercise sympatholysis is not entirely mediated by the production of nitric oxide.
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