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1 Physiology, Mayo Clinic, Rochester, Minnesota, United States
2 Anesthesiology, Mayo Clinic & Foundation, Rochester, Minnesota, United States
3 Biostatistics, Mayo Clinic, Rochester, Minnesota, United States
4 Dept. of Anesthesiology, Mayo Clinic, Rochester, Minnesota, United States
5 Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota, United States
6 Department of Clinical Neurophysiology, Institute of Clinical Neurosciences, Goteborg, Sweden
* To whom correspondence should be addressed. E-mail: charkoudian.nisha{at}mayo.edu.
Large inter-individual 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 which 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 L-NMMA. Baseline MSNA ranged from 9 to 38 bursts/min (13 to 68 bursts/100 heart beats). L-NMMA caused dose-dependent increases in AP and total peripheral resistance (TPR), and reflex decreases in CO and MSNA. Increases in AP with L-NMMA were greater in individuals with high MSNA (PANOVA < 0.05). For example, after 8.5 mg/kg L-NMMA, in the low MSNA subgroup (n=6, 28 ± 4 bursts/100 hb), AP increased 9 ± 1 mmHg, whereas in the high MSNA subgroup (n=6, 58 ± 3 bursts/100 hb) 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 TPR 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.
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