During systemic nitric oxide synthase inhibition with L-NMMA, individuals with high resting muscle sympathetic nerve activity had greater increases in arterial pressure compared to those with low activity (15 vs 9 mmHg; P<0.01).
Does systemic nitric oxide synthase inhibition with L-NMMA differentially affect arterial pressure and cardiac output in normotensive humans with high versus low resting muscle sympathetic nerve activity?
Individuals with high resting sympathetic nerve activity rely more heavily on nitric oxide-mediated vasodilation to maintain normal arterial pressure and cardiac output.
Absolute Event Rate: 15% vs 9%
p-value: p=<0.01
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 NG-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 (PANOVA<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.
Charkoudian et al. (Sat,) conducted a other in Normotension (n=12). High resting muscle sympathetic nerve activity (MSNA) vs. Low resting MSNA was evaluated on Increase in arterial pressure after 8.5 mg/kg of L-NMMA (p=<0.01). During systemic nitric oxide synthase inhibition with L-NMMA, individuals with high resting muscle sympathetic nerve activity had greater increases in arterial pressure compared to those with low activity (15 vs 9 mmHg; P<0.01).