Holwerda Seth W, Luehrs Rachel E, Gremaud Allene L, Wooldridge Nealy A, Stroud Amy K, Fiedorowicz Jess G, Abboud Francois M, Pierce Gary L
Department of Health and Human Physiology, University of Iowa , Iowa City, Iowa.
Abboud Cardiovascular Research Center, University of Iowa , Iowa City, Iowa.
J Neurophysiol. 2018 Jul 1;120(1):11-22. doi: 10.1152/jn.00064.2018. Epub 2018 Mar 14.
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.
肌肉交感神经活动(MSNA)的相对爆发幅度是交感神经输出增强的一个指标,并导致更强的血管收缩反应。有证据表明,惊恐障碍患者中焦虑会导致相对MSNA爆发幅度增加;因此,我们假设急性应激会导致慢性焦虑个体的相对MSNA爆发幅度增加和血管收缩。对18名慢性焦虑患者(ANX组;8名男性,10名女性,32±2岁)和18名低焦虑或无焦虑的健康对照者(CON组;8名男性,10名女性,39±3岁)进行了研究。ANX组和CON组的基线MSNA和24小时血压相似(P>0.05);然而,ANX组夜间收缩压的下降幅度减弱(P=0.02)。在紧接(预期)生理应激之前和期间(2分钟冷加压试验;ANX组:73±5 vs.CON组:59±3任意单位(AU),P=0.03)以及精神应激期间(4分钟心算;ANX组:65±3 vs.CON组:54±3%AU,P=0.02),ANX组的相对MSNA爆发幅度显著高于CON组。与CON组相比,ANX组对应激反应的MSNA爆发频率、发生率和总活动量没有增加(P>0.05),并且冷应激期间肱动脉传导率的降低在ANX组和CON组之间相似(P=0.92)。精神应激期间的相对MSNA爆发幅度与状态焦虑(P<0.01)和特质焦虑(P=0.01)(状态-特质焦虑量表)密切相关,与年龄、性别和体重指数无关。因此,在应对急性应激(包括精神应激和生理应激)时,慢性焦虑个体的相对MSNA爆发幅度会选择性增加,这表明在心血管疾病风险较高的人群中交感神经驱动增强。新发现与值得注意的点:慢性焦虑个体在应对急性精神和生理应激时,肌肉交感神经活动的相对爆发幅度会选择性增加,慢性焦虑是一种常见疾病,与心血管疾病的发生有关。在没有常见合并症的情况下,慢性焦虑会出现交感神经爆发幅度增加。这些发现为焦虑、急性应激和交感神经激活之间的关系提供了重要见解。