Rosenmeier, Jaya B

Nitric oxide (NO) is capable of blunting α-adrenergic vasoconstriction in contracting skeletal muscles of experimental animals (functional sympatholysis). We therefore tested the hypothesis that exogenous NO administration can blunt α-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 α-adrenergic constrictors (tyramine, which evokes endogenous norepinephrine release; phenylephrine, an α1-agonist; and clonidine, an α2-agonist). To simulate exercise hyperemia, the vasoconstriction caused by the α-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 α-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 α-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 α-adrenergic vasoconstriction in the resting human forearm.