(748.2) Obesity-related higher blood pressure is associated with augmented transduction of spontaneous muscle sympathetic nerve activity

Poster Board Number: E405

Seth Holwerda (University of Kansas Medical Center, University of Kansas Medical Center, University of Iowa), Megan Gangwish (University of Kansas Medical Center), Rachel Luehrs (North Central College), Virginia Nuckols (University of Iowa), Gary Pierce (University of Iowa, University of Iowa)

Central obesity is associated with elevated adrenergic activity and arterial blood pressure (BP). Therefore, we tested the hypothesis that transduction of spontaneous muscle sympathetic nerve activity (MSNA) to BP, i.e., sympathetic transduction, would be augmented in central obesity (increased waist circumference) and positively related to resting BP.  Young/middle-age obese (n=14) or non-obese (n=14) adults without hypertension (average ambulatory 24-hr BPlt;130/80 mmHg) were included. MSNA (microneurography) and BP (finger cuff) were measured continuously for 10 min (supine) and bursts of MSNA were grouped into quartiles of burst clusters (1, 2, 3, 4+bursts) and burst amplitude. Beat-to-beat mean arterial pressure (MAP) was signal-averaged over 10 cardiac cycles following each burst of MSNA. MSNA burst frequency was similar between obese and non-obese (21±3vs.17±3 bursts/min, P=0.34). However, supine BP was significantly higher in obese compared with non-obese (systolic: 127±3vs.114±3; diastolic: 76±2vs.64±1 mmHg, both Plt;0.01). Importantly, obese showed greater MAP responses to clusters of bursts compared with non-obese (e.g.,4th quartile: 4.5±0.4vs.3.3±0.4 mmHg, P=0.05), but did not show greater MAP responses to higher burst amplitude (P=0.13). MAP responses to clusters of bursts were positively correlated with systolic BP when controlling for age, sex, and MSNA (R=0.43, P=0.03), but this correlation was abolished when also controlling for BMI (R=0.20, P=0.34). Diastolic BP was only weakly correlated with MAP responses to clusters of bursts (R=0.27, P=0.20). These findings suggest that the pressor response to clustered bursts of MSNA (i.e., sympathetic transduction) is augmented in central obesity and may contribute to the obesity-related rise in supine systolic BP.

Funding and support: R01HL159370-01 (S.W.H.) and R01AG063790 (G.L.P.). This work was also supported by a CTSA grant from NCATS awarded to the University of Kansas for Frontiers: University of Kansas Clinical and Translational Science Institute (# UL1TR002366) and to the University of Iowa Institute for Clinical and Translational Science (# UL1TR002537). The contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH or NCATS.