Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 287, Issue 6, Pages H2576-H2584Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00621.2004
Keywords
nitric oxide; prostaglandin; exercise; blood flow; sympathetic nervous system
Funding
- NCRR NIH HHS [RR-00585] Funding Source: Medline
- NHLBI NIH HHS [HL-46493] Funding Source: Medline
- NIA NIH HHS [AG-05912, AG-22337] Funding Source: Medline
- NINDS NIH HHS [NS-32352] Funding Source: Medline
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Sympathetic alpha-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 alpha-adrenergic receptor stimulation during rhythmic handgrip exercise (6.4 kg) and during a control nonexercise vasodilator condition (using intraarterial 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 alpha(1)-agonist), and clonidine (an alpha(2)-agonist) were significantly blunted during exercise compared with adenosine treatment. After combined inhibition of NO and PGs, the vasoconstrictor responses to all alpha-adrenergic receptor stimuli were augmented by similar to10% in contracting muscle (P<0.05), whereas the responses to phenylephrine and clonidine were also augmented by similar to 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 alpha-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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