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-Adrenergic Vasoconstriction in Contracting Human Skeletal Muscle
1 Health and Exercise Science, Colorado State University, Fort Collins, CO, USA
2 Anesthesia Research, Mayo Clinic and Foundation, Rochester, MN, USA
* To whom correspondence should be addressed. E-mail: fdinenno{at}cahs.colostate.edu.
Sympathetic 
-adrenergic vasoconstrictor responses are blunted in the vascular beds of contracting muscle (functional sympatholysis). We tested the hypothesis that combined inhibition of nitric oxide (NO) and prostaglandins (PGs) restores sympathetic vasoconstriction in contracting human muscle. We measured forearm blood flow (Doppler ultrasound) and calculated the reductions in forearm vascular conductance (FVC) in response to -adrenergic receptor stimulation during rhythmic handgrip exercise (6.4 kg) and during a control non-exercise vasodilator condition (intra-arterial adenosine), before and after combined local inhibition of NO synthase (NOS; via NG-nitro-L-arginine methyl ester) and cyclooxygenase (COX; via ketorolac) in healthy men. Before combined inhibition of NO and PGs, the forearm vasoconstrictor responses to intra-arterial tyramine (evokes endogenous noradrenaline release), phenylephrine (selective 1-agonist), and clonidine (2-agonist) were significantly blunted during exercise compared with adenosine. After combined inhibition of NO and PGs, the vasoconstrictor responses to all -adrenergic receptor stimuli were augmented by ~10% in contracting muscle (P<0.05), whereas the responses to phenylephrine and clonidine were also augmented by ~10% during passive vasodilation in resting muscle (P<0.05). In 6 additional subjects, PG inhibition alone did not alter the vasoconstrictor responses in resting or contracting muscle. Thus, in light of our previous findings, it appears that inhibition of either NO or PGs alone does not impact on functional sympatholysis in healthy humans. However, the results from the present study indicate that combined inhibition of NO and PGs augments -adrenergic vasoconstriction in contracting muscle, but does not completely restore the vasoconstrictor responses compared with those observed during passive vasodilation in resting muscle.
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