α1- and α2-adrenergic vasoconstriction is blunted in contracting human muscle

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 alpha(1)- or alpha(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 a(1) agonist) and clonidine (an alpha(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 +/- 6vs. -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 alpha(2)-adrenergic receptor-mediated vasoconstrictor responses are much more sensitive to contraction-induced inhibition than alpha(1)-mediated responses. We conclude that vasoconstrictor responses mediated via both post-junctional alpha(1)- and alpha(2)-adrenergic receptors are blunted in contracting human skeletal muscles.