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Exogenous NO administration and alpha-adrenergic vasoconstriction in human limbs
Jaya B Rosenmeier1, Sandy J Fritzlar, Frank A Dinenno
1Department of Anesthesiology, Mayo Clinic, Rochester, MN 55905, USA.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|August 19, 2003
Summary
Exogenous nitric oxide (NO) administration does not blunt alpha-adrenergic vasoconstriction in resting human limbs, even when blood flow is elevated to simulate exercise hyperemia. This finding contrasts with observations in animal models regarding functional sympatholysis.
Area of Science:
- Cardiovascular Physiology
- Human Physiology
- Pharmacology
Background:
- Nitric oxide (NO) is known to blunt alpha-adrenergic vasoconstriction in animal skeletal muscles, a phenomenon termed functional sympatholysis.
- The role of exogenous NO in modulating alpha-adrenergic vasoconstriction in resting human limbs remains unclear.
- Understanding this interaction is crucial for comprehending vascular regulation and potential therapeutic interventions.
Purpose of the Study:
- To test the hypothesis that exogenous NO administration can blunt alpha-adrenergic vasoconstriction in resting human limbs.
- To investigate the effect of NO on vasoconstrictor responses to tyramine, phenylephrine, and clonidine.
- To compare NO-mediated and NO-independent vasodilation in the context of alpha-adrenergic constriction.
Main Methods:
- Eight healthy males participated in the study.
- Forearm blood flow (FBF) and blood pressure were measured using Doppler ultrasound.
- Brachial artery infusions of adenosine (NO-independent) and sodium nitroprusside (SNP, NO donor) were used to induce vasodilation.
- Infusions of tyramine, phenylephrine, and clonidine were administered to assess alpha-adrenergic vasoconstriction during both vasodilation conditions.
Main Results:
- Both adenosine and SNP significantly increased FBF, simulating exercise hyperemia.
- All three alpha-adrenergic constrictors (tyramine, phenylephrine, clonidine) caused significant reductions in FBF and forearm vascular conductance.
- Relative reductions in forearm vascular conductance during SNP infusion were similar or slightly greater compared to adenosine, indicating no blunting effect of exogenous NO.
Conclusions:
- Exogenous NO administration, at levels simulating exercise hyperemia, does not blunt alpha-adrenergic vasoconstriction in the resting human forearm.
- The findings suggest that functional sympatholysis, as observed in animal models, may not directly translate to resting human limbs.
- Further research is needed to elucidate the precise mechanisms of vascular control in human limbs under conditions of NO availability and sympathetic activation.