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 Women with a history of preeclampsia (hxPE) exhibit sustained arterial stiffness and elevated blood pressure (BP) postpartum. Aortic stiffness and 24-hour BP variability (BPV) are associated with age-related cognitive decline. Although hxPE is related to altered cognitive function, the association between aortic stiffness and BPV with cognitive performance in young women with hxPE has not been investigated. The objectives of this study were to 1) test whether cognitive performance is lower in young women with hxPE and 2) determine whether aortic stiffness and BPV are associated with cognitive performance independent of 24-hour average BP. Methods Women with hxPE (N=23) and healthy pregnancy controls (N=38) were enrolled 1-3 years postpartum. Cognitive performance was assessed in domains of memory, processing speed and executive function. 24-hour ambulatory BP monitoring and carotid-femoral pulse wave velocity (cfPWV) were used to measure BPV and aortic stiffness, respectively. Results Women with hxPE had slower processing speed (-0.56±0.17 versus 0.34±0.11 Z-score, P&lt;0.001) and lower executive function (-0.43±0.14 versus 0.31±0.10 Z-score, P=0.004) compared with controls independent of education, whereas memory did not differ. BPV and cfPWV (adjusted for BP) did not differ between women with hxPE and controls. Greater diastolic BPV was associated with lower executive function independent of 24-hour average BP and education in women with hxPE (r = -0.48, P=0.03) but not controls (r = 0.15, P=0.38). Conclusions Select cognitive functions are reduced postpartum in young women with a recent hxPE and linked with elevated 24-hour diastolic BPV.

Women with preeclampsia, a hypertensive disorder of pregnancy, exhibit greater beat-to-beat blood pressure variability (BPV) in the third trimester after clinical onset of the disorder. However, it remains unknown whether elevated BPV precedes the development of preeclampsia. A prospective study cohort of 139 women (age 30.2±4.0 years) were enrolled in early pregnancy (<14 weeks gestation). BPV was quantified by time domain analyses of 10-minute continuous beat-to-beat blood pressure recordings via finger photoplethysmography in the first, second, and third trimesters. Aortic stiffness (carotid-femoral pulse wave velocity) and spontaneous cardiovagal baroreflex sensitivity were also measured each trimester. Eighteen women (13%) developed preeclampsia. Systolic BPV was higher in all trimesters among women who developed versus did not develop preeclampsia (first: 4.8±1.3 versus 3.7±1.2, P =0.001; second: 5.1±1.8 versus 3.8±1.1, P =0.02; third: 5.2±0.8 versus 4.0±1.1 mm Hg, P =0.002). Elevated first trimester systolic BPV was associated with preeclampsia (odds ratio, 1.94 [95% CI, 1.27–2.99]), even after adjusting for risk factors (age, body mass index, systolic blood pressure, history of preeclampsia, and diabetes mellitus) and was a significant predictor of preeclampsia (area under the receiver operator characteristic curve=0.75±0.07; P =0.002). Carotid-femoral pulse wave velocity was elevated in the first trimester among women who developed preeclampsia (5.9±0.8 versus 5.2±0.8 m/s; P =0.002) and was associated with BPV after adjustment for mean blood pressure ( r =0.26; P =0.005). First trimester baroreflex sensitivity did not differ between groups ( P =0.23) and was not related to BPV ( P =0.36). Elevated systolic BPV is independently associated with the development of preeclampsia as early as the first trimester, possibly mediated in part by higher aortic stiffness.

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