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Exogenous NO administration and -adrenergic vasoconstriction in human limbs

Department of Anesthesiology and General Clinical Research Center, Mayo Clinic and Foundation, Rochester, Minnesota 55905

Submitted 18 June 2003 ; accepted in final form 11 August 2003

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 eight healthy males during brachial artery infusions of three -adrenergic constrictors (tyramine, which evokes endogenous norepinephrine release; phenylephrine, an ₁-agonist; and clonidine, an 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 to 200–250 ml/min. All three -adrenergic constrictor drugs caused marked reductions in FBF and calculated forearm vascular conductance (P < 0.05). The relative reductions in forearm vascular conductance caused by the -adrenergic constrictors during SNP infusion were similar (tyramine, –74 ± 3 vs. –65 ± 2%; 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.

functional sympatholysis; sympathetic nervous system; sympathetic modulation; nitric oxide

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