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Role of Nitric Oxide and -Adrenergic Receptor Responsiveness in Exercising Skeletal Muscle

Department of General Internal Medicine
Section of Gerontology & Geriatrics
Leiden University Medical Center
2300 RC Leiden, The Netherlands
E-mail:a.m.kamper{at}lumc.nl

ABSTRACT

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 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. Before nitric oxide synthase inhibition with N^G-nitro-L-arginine methyl ester L-NAME), intra-arterial infusions of phenylephrine elicited reductions in vascular conductance of –91 ± 3, –80 ± 5, and –75 ± 6% (means ± SE) at rest, 3 miles/h, and 6 miles/h and 10% grade, respectively. Intra-arterial clonidine reduced vascular conductance by –65 ± 6, –39 ± 4, and –30 ± 3%. After L-NAME, intra-arterial infusions of phenylephrine elicited reductions in vascular conductance of –85 ± 5, –85 ± 5, and –84 ± 5%, whereas clonidine reduced vascular conductance by –67 ± 5, –45 ± 3, and –35 ± 3%, at rest, 3 miles/h, and 6 miles/h and 10% grade. ₁-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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Medical College of Wisconsin/Veterans Affairs Medical Center
Milwaukee, Wisconsin 53226