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This Article Full Text Full Text (PDF) All Versions of this Article: 287/6/H2576    most recent 00621.2004v1 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 ISI 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 ISI Web of Science (11) Citing Articles via Google Scholar Google Scholar Articles by Dinenno, F. A. Articles by Joyner, M. J. Search for Related Content PubMed PubMed Citation Articles by Dinenno, F. A. Articles by Joyner, M. J.

Combined NO and PG inhibition augments -adrenergic vasoconstriction in contracting human skeletal muscle

¹Department of Health and Exercise Science, Colorado State University, Fort Collins, Colorado 80523-1582; and ²Department of Anesthesiology and General Clinical Research Center, Mayo Clinic and Foundation, Rochester, Minnesota 55905

Submitted 23 June 2004 ; accepted in final form 15 July 2004

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 via Doppler ultrasound and calculated the reduction in forearm vascular conductance in response to -adrenergic receptor stimulation during rhythmic handgrip exercise (6.4 kg) and during a control nonexercise vasodilator condition (using intra-arterial adenosine) before and after combined local inhibition of NO synthase (NOS; via N^G-nitro-L-arginine methyl ester) and cyclooxygenase (via ketorolac) in healthy men. Before combined inhibition of NO and PGs, the forearm vasoconstrictor responses to intra-arterial tyramine (which evoked endogenous noradrenaline release), phenylephrine (a selective ₁-agonist), and clonidine (an ₂-agonist) were significantly blunted during exercise compared with adenosine treatment. 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 six additional subjects, PG inhibition alone did not alter the vasoconstrictor responses in resting or contracting muscles. Thus in light of our previous findings, it appears that inhibition of either NO or PGs alone does not affect 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.

nitric oxide; prostaglandin; exercise; blood flow; sympathetic nervous system

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