Muscle sympathetic neural activity (MSNA) influences the mechanical properties (i.e., vascular smooth muscle tone and stiffness) of peripheral arteries, but it remains controversial whether MSNA contributes to stiffness of central arteries such as the aorta and carotids. We examined whether elevated MSNA (age-related) would be independently associated with greater stiffness of central [carotid-femoral pulse wave velocity (PWV)] and peripheral (carotid-brachial PWV) arteries, in addition to lower carotid compliance coefficient (CC), in healthy men and women (n=88, age:19-73 years, 52%men). Also, we examined whether acute elevations in MSNA without increases in mean arterial pressure (MAP) using graded levels of lower body negative pressure (LBNP) would augment central and peripheral artery stiffness in young (YG, n=15, 60%men) and middle-age/older adults (MA/O, n=14, 43%men). Resting MSNA burst frequency (bursts•min −1) was significantly correlated with carotid-femoral PWV (R=0.44, P<0.001), carotid-brachial PWV (R=0.32, P=0.003), and carotid CC (R=0.28, P=0.01) after controlling for sex, MAP, heart rate, and waist-to-hip ratio (central obesity), but these correlations were abolished after further controlling for age (all P>0.05). In YG and MA/O adults, MSNA was elevated during LBNP (P<0.001) and produced significant increases in carotid-femoral PWV (YG:Δ+1.3±0.3 vs. MA/ O:Δ+1.0±0.3 m•s −1 , P=0.53) and carotid-brachial PWV (YG: Δ+0.7±0.3 vs. MA/O: Δ+0.7±0.5 m•s −1 , P=0.92), whereas carotid CC during LBNP was significantly reduced in YG but not MA/O (YG:Δ-0.04 ±0.01 vs. MA/O:Δ0.001±0.008 mm 2 •mmHg −1 , P<0.01). Collectively, these data demonstrate the influence of MSNA on central artery stiffness and its potential contribution to age-related increases in stiffness of both peripheral and central arteries.

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.

Background The associations of chronic cigarette smoking with blood pressure (BP) remain mixed. It is unclear whether a lack of examination of racial differences contributed to the mixed findings in previous studies. Black smokers metabolize nicotine at a slower rate than White smokers and racial discrimination contributes to nicotine dependence and higher BP among Black smokers. Methods and Results We studied the association between cigarette smoking and longitudinal (30‐year) changes in systolic BP, diastolic BP, and pulse pressure (PP) in 4786 Black and White individuals from the CARDIA (Coronary Artery Risk Development in Young Adults) study using repeated‐measures regression models. Neither systolic BP, nor diastolic BP differed between Black consistent smokers compared with Black never smokers, although Black consistent smokers had higher PP than Black never smokers (β=1.01 mm Hg, P =0.028). White consistent smokers had similar systolic BP, but lower diastolic BP (β=−2.27 mm Hg, P <0.001) and higher PP (β=1.59 mm Hg, P <0.001) compared with White never smokers. There were no differences in systolic BP, diastolic BP, or PP between Black or White long‐term former smokers compared with never smokers (all P >0.05). Conclusions Although the associations of cigarette smoking with alterations in BP are small, the greater PP observed in consistent smokers may contribute in part to the higher cardiovascular disease risk observed in this group because PP is a strong predictor of cardiovascular disease risk after middle age.

Aging is characterized by increased wall thickness of the central elastic arteries (i.e., aorta and carotid arteries), although the mechanisms involved are unclear. Evidence suggests that age-related increases in muscle sympathetic nerve activity (MSNA) may be a contributing factor. However, studies in humans have been lacking. Therefore, we tested the hypothesis that age-related increases in MSNA would be independently associated with carotid artery intima-media thickness (IMT) but not in young women given the reduced influence of MSNA on the vasculature in this group. In 93 young and middle-age/older (MA/O) adults (19–73 yr, 41 women), we performed assessments of MSNA (microneurography) and common carotid IMT and lumen diameter (ultrasonography). Multiple regression that included MSNA and other cardiovascular disease risk factors indicated that MSNA ( P = 0.002) and 24-h systolic blood pressure (BP) ( P = 0.024) were independent determinants of carotid IMT-to-lumen ratio (model R2 = 0.38, P < 0.001). However, when examining only young women (<45 yr), no correlation was observed between MSNA and carotid IMT-to-lumen ratio ( R = −0.01, P = 0.963). MSNA was significantly correlated with IMT-to-lumen ratio while controlling for 24-h systolic BP among young men ( R = 0.49, P < 0.001) and MA/O women ( R = 0.59, P = 0.022). However, among MA/O men, controlling for 24-h systolic BP attenuated the association between MSNA and carotid IMT-to-lumen ratio ( R = 0.50, P = 0.115). Significant age differences in IMT-to-lumen ratio between young and MA/O men ( P = 0.047) and young and MA/O women ( P = 0.023) were removed when adjusting for MSNA (men: P = 0.970; women: P = 0.152). These findings demonstrate an association between higher sympathetic outflow and carotid artery wall thickness with a particular exception to young women. NEW & NOTEWORTHY Increased wall thickness of the large elastic arteries serves as a graded marker for cardiovascular disease risk and progression of atherosclerosis. Findings from the present study establish an independent association between higher sympathetic outflow and carotid artery wall thickness in adults with an exception to young women and extend findings from animal models that demonstrate hypertrophy of vascular smooth muscle following chronic sympathetic-adrenergic stimulation.