| Autor: |
Holwerda SW; Department of Health and Human Physiology, University of Iowa , Iowa City, Iowa.; Abboud Cardiovascular Research Center, University of Iowa , Iowa City, Iowa., Luehrs RE; Department of Health and Human Physiology, University of Iowa , Iowa City, Iowa., Gremaud AL; Department of Health and Human Physiology, University of Iowa , Iowa City, Iowa., Wooldridge NA; Department of Health and Human Physiology, University of Iowa , Iowa City, Iowa., Stroud AK; Department of Psychiatry, University of Iowa , Iowa City, Iowa., Fiedorowicz JG; Department of Psychiatry, University of Iowa , Iowa City, Iowa.; Department of Epidemiology, University of Iowa , Iowa City, Iowa.; Department of Internal Medicine, University of Iowa , Iowa City, Iowa.; Abboud Cardiovascular Research Center, University of Iowa , Iowa City, Iowa., Abboud FM; Department of Internal Medicine, University of Iowa , Iowa City, Iowa.; Department of Molecular Physiology and Biophysics, University of Iowa , Iowa City, Iowa.; Abboud Cardiovascular Research Center, University of Iowa , Iowa City, Iowa., Pierce GL; Department of Health and Human Physiology, University of Iowa , Iowa City, Iowa.; Abboud Cardiovascular Research Center, University of Iowa , Iowa City, Iowa.; Fraternal Order of Eagles Diabetes Research Center, University of Iowa , Iowa City, Iowa. |
| Abstrakt: |
Relative burst amplitude of muscle sympathetic nerve activity (MSNA) is an indicator of augmented sympathetic outflow and contributes to greater vasoconstrictor responses. Evidence suggests anxiety-induced augmentation of relative MSNA burst amplitude in patients with panic disorder; thus we hypothesized that acute stress would result in augmented relative MSNA burst amplitude and vasoconstriction in individuals with chronic anxiety. Eighteen participants with chronic anxiety (ANX; 8 men, 10 women, 32 ± 2 yr) and 18 healthy control subjects with low or no anxiety (CON; 8 men, 10 women, 39 ± 3 yr) were studied. Baseline MSNA and 24-h blood pressure were similar between ANX and CON ( P > 0.05); however, nocturnal systolic blood pressure % dipping was blunted among ANX ( P = 0.02). Relative MSNA burst amplitude was significantly greater among ANX compared with CON immediately preceding (anticipation) and during physiological stress [2-min cold pressor test; ANX: 73 ± 5 vs. CON: 59 ± 3% arbitrary units (AU), P = 0.03] and mental stress (4-min mental arithmetic; ANX: 65 ± 3 vs. CON: 54 ± 3% AU, P = 0.02). Increases in MSNA burst frequency, incidence, and total activity in response to stress were not augmented among ANX compared with CON ( P > 0.05), and reduction in brachial artery conductance during cold stress was similar between ANX and CON ( P = 0.92). Relative MSNA burst amplitude during mental stress was strongly correlated with state ( P < 0.01) and trait ( P = 0.01) anxiety (State-Trait Anxiety Inventory), independent of age, sex, and body mass index. Thus in response to acute stress, both mental and physiological, individuals with chronic anxiety demonstrate selective augmentation in relative MSNA burst amplitude, indicating enhanced sympathetic drive in a population with higher risk for cardiovascular disease. NEW & NOTEWORTHY Relative burst amplitude of muscle sympathetic nerve activity in response to acute mental and physiological stress is selectively augmented in individuals with chronic anxiety, which is a prevalent condition that is associated with the development of cardiovascular disease. Augmented sympathetic burst amplitude occurs with chronic anxiety in the absence of common comorbidities. These findings provide important insight into the relation between anxiety, acute stress and sympathetic activation. |
