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-adrenergic vasoconstriction in human limbs
1 Anesthesiology, Mayo Clinic, Rochester, MN, USA
2 Anesthesiology, Mayo Clinic, Rochester, MN, USA; General Clinical Research Center, Mayo Clinic, Rochester, MN, USA
* To whom correspondence should be addressed. E-mail: joyner.michael{at}mayo.edu.
Nitric oxide (NO) is capable of blunting 
-adrenergic vasoconstriction in contracting skeletal muscles of experimental animals (functional sympatholysis). We therefore tested the hypothesis that exogenous NO administration can blunt -adrenergic vasoconstriction in resting human limbs by measuring forearm blood flow (FBF; Doppler ultrasound) and blood pressure in 8 healthy males during brachial artery infusions of three -adrenergic constrictors (tyramine = evokes endogenous NE release; phenylephrine = 1 agonist; clonidine = 2-agonist). To simulate exercise hyperemia, the vasoconstriction caused by the -agonists was compared during adenosine-mediated (>50% NO independent) and sodium nitroprusside-mediated (SNP; NO donor) vasodilation of the forearm. Both adenosine and SNP increased FBF from ~35-40 ml[[rad]]min-1 to ~200-250 ml[[rad]]min-1. All three -adrenergic constrictor drugs caused marked reductions in FBF and calculated forearm vascular conductance (FVC; P<0.05). The relative reductions in FVC caused by the -adrenergic constrictors during SNP infusion were similar (tyramine = -74±3 vs -652±%; clonidine = -44±6 vs -44±6%; P>0.05), or slightly greater (phenylephrine = -47±6 vs -33±6%; P<0.05) compared with the responses during adenosine. In conclusion, these results indicate that exogenous NO sufficient to raise blood flow to levels simulating those seen during exercise does not blunt -adrenergic vasoconstriction in the resting human forearm.
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