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This Article Full Text Full Text (PDF) All Versions of this Article: 291/3/H1378    most recent 00234.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (10) Citing Articles via Google Scholar Google Scholar Articles by Charkoudian, N. Articles by Wallin, B. G. Search for Related Content PubMed PubMed Citation Articles by Charkoudian, N. Articles by Wallin, B. G.

Relationship between muscle sympathetic nerve activity and systemic hemodynamics during nitric oxide synthase inhibition in humans

¹Department of Physiology and Biomedical Engineering, ²Department of Anesthesiology and ³General Clinical Research Center, Mayo Clinic College of Medicine, Rochester, Minnesota; and ⁴Institute of Clinical Neurosciences, Göteborg University, Göteborg, Sweden

Submitted 7 March 2006 ; accepted in final form 20 April 2006

Large interindividual differences exist in resting sympathetic nerve activity (SNA) among normotensive humans with similar arterial pressure (AP). We recently showed inverse relationships of resting SNA with cardiac output (CO) and vascular adrenergic responsiveness that appear to balance the influence of differences in SNA on blood pressure. In the present study, we tested whether nitric oxide (NO)-mediated vasodilation has a role in this balance by evaluating hemodynamic responses to systemic NO synthase (NOS) inhibition in individuals with low and high resting muscle SNA (MSNA). We measured MSNA via peroneal microneurography, CO via acetylene uptake and AP directly, at baseline and during increasing systemic doses of the NOS inhibitor N^G-monomethyl-L-arginine (L-NMMA). Baseline MSNA ranged from 9 to 38 bursts/min (13 to 68 bursts/100 heartbeats). L-NMMA caused dose-dependent increases in AP and total peripheral resistance and reflex decreases in CO and MSNA. Increases in AP with L-NMMA were greater in individuals with high baseline MSNA (P_ANOVA < 0.05). For example, after 8.5 mg/kg of L-NMMA, in the low MSNA subgroup (n = 6, 28 ± 4 bursts/100 heartbeats), AP increased 9 ± 1 mmHg, whereas in the high-MSNA subgroup (n = 6, 58 ± 3 bursts/100 heartbeats), AP increased 15 ± 2 mmHg (P < 0.01). The high-MSNA subgroup had lower baseline CO and smaller decreases in CO with L-NMMA, but changes in total peripheral resistance were not different between groups. We conclude that differences in CO among individuals with varying sympathetic traffic have important hemodynamic implications during disruption of NO-mediated vasodilation.

hypertension; cardiac output; sympathetic nervous system

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