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Augmented pressor responses to individual bursts of muscle sympathetic nerve activity in human obesity
Author(s) -
Holwerda Seth,
Luehrs Rachel,
Nuckols Virginia,
Pierce Gary
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.05364
Subject(s) - microneurography , medicine , blood pressure , endocrinology , obesity , sympathetic nervous system , cardiology , baroreflex , heart rate
Obesity is associated with increased sympathetic outflow and hypertension. However, it remains unclear whether the systemic pressor response to spontaneous bursts of sympathetic nerve activity (i.e., sympathetic transduction) is augmented in obesity. Therefore, we tested the hypothesis that transduction of muscle sympathetic nerve activity (MSNA) to arterial blood pressure (BP) is significantly higher in obese vs. lean adults. Also, because obesity alters regulation of BP over the 24‐hour period, we further examined the extent to which sympathetic transduction is associated with ambulatory 24‐hour BP variability (standard deviation). MSNA (microneurography) and arterial BP (finger cuff) were measured continuously for 10 min under resting conditions in 20 young/middle‐age obese participants and 20 age‐ and sex‐matched lean controls. Signal averaging was used to characterize beat‐by‐beat changes in mean arterial pressure (MAP) for 15 cardiac cycles following each MSNA burst. MSNA was not significantly elevated in obese vs. lean participants (25±11 vs. 21±10 bursts/min, P=0.27). However, transduction of MSNA to BP was significantly elevated in obese vs. lean participants when considering multiple successive bursts (P<0.01) and all bursts (P<0.01). Similarly, increases in burst amplitude evoked greater MAP responses with obese having the largest peak increases (3.8±1.7 vs. 2.7±1.6 mmHg, P=0.03). Multiple regression indicated that sympathetic transduction was a significant determinant of 24‐hour MAP variability (β=0.47, P<0.01), independent of age, BMI, MSNA, and 24‐hour MAP (all P>0.05). These findings demonstrate that transduction of MSNA to BP is augmented in human obesity. Sympathetic transduction also appears to contribute to higher BP variability independent of obesity.