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J Physiol Volume 572, Number 3, 821-827, May 1, 2006 DOI: 10.1113/jphysiol.2005.104075
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Cardiovascular

Vascular adrenergic responsiveness is inversely related to tonic activity of sympathetic vasoconstrictor nerves in humans

N. Charkoudian1,2, M. J. Joyner2, L. A. Sokolnicki1,2, C. P. Johnson2, J. H. Eisenach2, N. M. Dietz2, T. B. Curry2 and B. G. Wallin3

1 Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, USA
2 Departments of Anaesthesiology, Mayo Clinic, Rochester, MN, USA
3 Institute of Clinical Neurosciences, Göteborg University, Göteborg, Sweden

In humans, sympathetic nerve activity (SNA) at rest can vary several-fold among normotensive individuals with similar blood pressures. We recently showed that a balance exists between SNA and cardiac output, which may contribute to the maintenance of normal blood pressures over the range of resting SNA levels. In the present studies, we assessed whether variability in vascular adrenergic responsiveness has a role in this balance. We tested the hypothesis that forearm vascular responses to noradrenaline (NA) and tyramine (TYR) are related to SNA such that individuals with lower resting SNA have greater adrenergic responsiveness, and vice-versa. We measured multifibre muscle SNA (MSNA; microneurography), arterial pressure (brachial catheter) and forearm blood flow (plethysmography) in 19 healthy subjects at baseline and during intrabrachial infusions of NA and TYR. Resting MSNA ranged from 6 to 34 bursts min–1, and was inversely related to vasoconstrictor responsiveness to both NA (r= 0.61, P= 0.01) and TYR (r= 0.52, P= 0.02), such that subjects with lower resting MSNA were more responsive to NA and TYR. We conclude that interindividual variability in vascular adrenergic responsiveness contributes to the balance of factors that maintain normal blood pressure in individuals with differing levels of sympathetic neural activity. Further understanding of this balance may have important implications for our understanding of the pathophysiology of hypertension.

(Received 20 December 2005; accepted after revision 1 March 2006; first published online 2 March 2006)
Corresponding author N. Charkoudian: Department of Physiology and Biomedical Engineering, JO-4184W, Mayo Clinic College of Medicine, Rochester, MN 55905, USA. Email: charkoudian.nisha{at}mayo.edu




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