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Sympathetic Baroreflex Sensitivity During Mental Stress in Humans With Chronic Anxiety
Author(s) -
Holwerda Seth W.,
Gremaud Allene L.,
Luehrs Rachel E.,
Fiedorowicz Jess G.,
Abboud Francois M.,
Pierce Gary L.
Publication year - 2018
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.2018.32.1_supplement.595.6
Subject(s) - baroreflex , medicine , anxiety , blood pressure , cardiology , heart rate , diastole , sympathetic nervous system , psychiatry
Elevated muscle sympathetic nerve activity (MSNA) is associated with the pathogenesis of hypertension and cardiac arrhythmias, and may be related to greater cardiovascular disease (CVD) risk among individuals with chronic anxiety. Augmented sympathetic responsiveness in chronic anxiety may potentially be attributed to alteration in sympathetic baroreflex control. We hypothesized that MSNA and its responsiveness to stress would be augmented in chronic anxiety, and that augmented MSNA responsiveness would be related to impaired sympathetic baroreflex sensitivity. Sympathetic baroreflex sensitivity was assessed by relating spontaneous changes in multi‐unit MSNA to beat‐to‐beat changes in diastolic blood pressure (DBP) using a weighted linear regression at rest (10 min) and during mental stress (MS, 4‐min mental arithmetic) in 18 individuals with moderate/high chronic anxiety (ANX, 6 men/12 women; 32±2 yrs; 27±2 kg/m 2 ) who were nonsmokers and free of CVD, and in 18 healthy controls with low/no anxiety (CON, 8 men/10 women; 39±3 yrs; 30±1 kg/m 2 ). Resting MSNA was not elevated among ANX compared to CON (MSNA burst incidence: ANX 29 ± 5 vs. CON 40 ± 4 bursts/100hb; Avg. relative MSNA burst amplitude: ANX 48 ± 1 vs. CON 47 ± 1 AU). Avg. relative MSNA burst amplitude in response to MS was significantly augmented among ANX compared to CON (ANX: 61 ± 2 vs. CON: 54 ± 2 AU, P=0.02), while % change in MSNA burst incidence was not significantly different between ANX and CON (ANX: 4 ± 7 vs. CON: 6 ± 7 bursts/100hb, P=0.86). Increases in avg. relative MSNA burst amplitude during MS were significantly correlated with trait anxiety score among all participants after adjusting for age, sex, and BMI (R=0.48, P=0.01). The slope between MSNA burst incidence and DBP was not different between ANX and CON at rest (ANX: −2.8 ± 0.6 vs. CON: −3.5 ± 0.5 bursts/100hb/mmHg −1 , P=0.35), and was significantly reduced during MS (P=0.03) with no difference between ANX and CON (ANX: −2.2 ± 0.4 vs. CON: −2.3 ± 0.5 bursts/100hb/mmHg −1 , P=0.42). The slope between total MSNA and diastolic BP was similar between ANX and CON at rest (ANX: −1.5 ± 0.3 vs. CON: −1.9 ± 0.3 AU/beat/mmHg −1 , P=0.3) and unchanged (P=0.49) during MS (ANX: −1.5 ± 0.3 vs. CON: −1.5 vs. 0.3 AU/beat/mmHg −1 , P=0.99). These preliminary findings demonstrate that individuals with chronic anxiety exhibit augmented increases in MSNA burst amplitude but not burst incidence to mental stress, and this alteration in the MSNA response to mental stress in chronic anxiety is not a result of impairment in sympathetic baroreflex sensitivity. Support or Funding Information AHA 17POST33440101, T32 HL07121 NHLBI (P01HL014388), U54 TR001356 and AHA (13DG143400012) This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .