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

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 BP<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 P<0.01). Importantly, obese showed greater MAP responses to clusters of bursts compared with non-obese (e.g.,4 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.