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Received December 17, 2002
Accepted after revision February 5, 2003
1- and 2-adrenergic vasoconstriction is blunted in contracting human muscle
1 Department of Anesthesiology and General Clinical Research Center, Mayo Clinic and Foundation, 200 First Street SW, Rochester, MN 55905, USA
2 Department of Anesthesiology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
* To whom correspondence should be addressed. E-mail: joyner.michael{at}mayo.edu.
Sympathetic vasoconstriction is blunted in the vascular beds of contracting skeletal muscles. We sought to determine whether this blunted vasoconstriction is specific for post-junctional 
1- or 2-adrenergic receptors. We measured forearm blood flow (Doppler ultrasound) and calculated the vascular conductance (FVC) responses to brachial artery infusions of tyramine (which evokes endogenous noradrenaline release), phenylephrine (an 1 agonist) and clonidine (an 2 agonist) in 10 healthy men during rhythmic handgrip exercise (10-15 % of maximum) and during a control non-exercise vasodilator condition (intra-arterial adenosine). Steady-state FVC during exercise and adenosine was similar in all trials (range: 243-272 and 234-263 ml min-1 (100 mmHg)-1, respectively; P > 0.5). During exercise the percentage reductions in FVC in response to tyramine (-24 ± 7 vs. -55 ± 6 %), phenylephrine (-12 ± 8 vs. -37 ± 8 %) and clonidine (-17 ± 6 vs. -49 ± 4 %) were significantly less compared with adenosine (all P < 0.05). The magnitude of the blunted vasoconstrictor responses was similar for both receptor subtypes. These findings are in contrast to those from studies in animals demonstrating that 2-adrenergic receptor-mediated vasoconstrictor responses are much more sensitive to contraction-induced inhibition than 1-mediated responses. We conclude that vasoconstrictor responses mediated via both post-junctional 1- and 2-adrenergic receptors are blunted in contracting human skeletal muscles.
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