scholarly journals Neurovascular responses to mental stress in prehypertensive humans

2011 ◽  
Vol 110 (1) ◽  
pp. 76-82 ◽  
Author(s):  
Christopher E. Schwartz ◽  
John J. Durocher ◽  
Jason R. Carter
Keyword(s):  
Heart Rate ◽  
Mental Stress ◽  
Sympathetic Nerve Activity ◽  
Mental Arithmetic ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Vascular Responses ◽  
Forearm Vascular Conductance

Neurovascular responses to mental stress have been linked to several cardiovascular diseases, including hypertension. Mean arterial pressure (MAP), muscle sympathetic nerve activity (MSNA), and forearm vascular responses to mental stress are well documented in normotensive (NT) subjects, but responses in prehypertensive (PHT) subjects remain unclear. We tested the hypothesis that PHT would elicit a more dramatic increase of MAP during mental stress via augmented MSNA and blunted forearm vascular conductance (FVC). We examined 17 PHT (systolic 120–139 and/or diastolic 80–89 mmHg; 22 ± 1 yr) and 18 NT (systolic < 120 and diastolic < 80 mmHg; 23 ± 2 yr) subjects. Heart rate, MAP, MSNA, FVC, and calf vascular conductance were measured during 5 min of baseline and 5 min of mental stress (mental arithmetic). Mental stress increased MAP and FVC in both groups, but the increases in MAP were augmented (Δ 10 ± 1 vs. Δ14 ± 1 mmHg; P < 0.05), and the increases in FVC were blunted (Δ95 ± 14 vs. Δ37 ± 8%; P < 0.001) in PHT subjects. Mental stress elicited similar increases in MSNA (Δ7 ± 2 vs. Δ6 ± 2 bursts/min), heart rate (Δ21 ± 3 vs. Δ18 ± 3 beats/min), and calf vascular conductance (Δ29 ± 10 vs. Δ19 ± 5%) in NT and PHT subjects, respectively. In conclusion, mental stress elicits an augmented pressor response in PHT subjects. This augmentation appears to be associated with altered forearm vascular, but not MSNA, responses to mental stress.

Gly16 + Glu27 β2-adrenoceptor polymorphisms cause increased forearm blood flow responses to mental stress and handgrip in humans

2005 ◽  
Vol 98 (3) ◽  
pp. 787-794 ◽  
Author(s):  
Ivani C. Trombetta ◽  
Luciana T. Batalha ◽  
Maria U. P. B. Rondon ◽  
Mateus C. Laterza ◽  
Eliana Frazzatto ◽  
...  
Keyword(s):  
Blood Flow ◽  
Sympathetic Nerve ◽  
Mental Stress ◽  
Sympathetic Nerve Activity ◽  
Forearm Blood Flow ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Exercise ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Forearm Vascular Conductance

We hypothesized that the muscle vasodilatation during mental stress and exercise would vary among humans who are polymorphic at alleles 16 and 27 of the β2-adrenoceptors. From 216 preselected volunteers, we studied 64 healthy, middle-aged normotensive women selected to represent three genotypes: homozygous for the alleles Arg16 and Gln27 (Arg16/Gln27, n = 34), Gly16 and Gln27 (Gly16/Gln27, n = 20), and Gly16 and Glu27 (Gly16/Glu27, n = 10). Forearm blood flow (plethysmography) and muscle sympathetic nerve activity (microneurography) were recorded during 3-min Stroop color-word test and 3-min handgrip isometric exercise (30% maximal voluntary contraction). Baseline muscle sympathetic nerve activity, forearm vascular conductance, mean blood pressure, and heart rate were not different among groups. During mental stress, the peak forearm vascular conductance responses were greater in Gly16/Glu27 group than in Gly16/Gln27 and Arg16/Gln27 groups (1.79 ± 0.66 vs. 0.70 ± 0.11 and 0.58 ± 0.12 units, P = 0.03). Similar results were found during exercise (0.80 ± 0.25 vs. 0.28 ± 0.08 and 0.31 ± 0.08 units, P = 0.02). Further analysis in a subset of subjects showed that brachial intra-arterial propranolol infusion abolished the difference in vasodilatory response between Gly16/Glu27 ( n = 6) and Arg16/Gln27 ( n = 7) groups during mental stress (0.33 ± 0.20 vs. 0.46 ± 0.21 units, P = 0.50) and exercise (0.08 ± 0.06 vs. 0.03 ± 0.03 units, P = 0.21). Plasma epinephrine concentration in Arg16/Gln27 and Gly16/Glu27 groups was similar. In conclusion, women who are homozygous for Gly16/Glu27 of the β2-adrenoceptors have augmented muscle vasodilatory responsiveness to mental stress and exercise.

Sex differences in sympathetic neural and limb vascular reactivity to mental stress in humans

2013 ◽  
Vol 304 (3) ◽  
pp. H436-H443 ◽  
Author(s):  
Huan Yang ◽  
Thomas D. Drummer ◽  
Jason R. Carter
Keyword(s):  
Blood Flow ◽  
Mental Stress ◽  
Vascular Reactivity ◽  
Sympathetic Nerve Activity ◽  
Forearm Blood Flow ◽  
Muscle Sympathetic Nerve Activity ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Men And Women ◽  
Forearm Vascular Conductance

Mental stress elicits a robust and consistent forearm vasodilation, but vascular reactivity in the calf remains inconsistent. It has been reported that calf vascular responses to MS may be sex dependent. Muscle sympathetic nerve activity (MSNA) is an important contributor to calf blood flow (CBF), yet the relations between sex, limb blood flow, and MSNA reactivity to mental stress have not been explored. We hypothesized that mental stress would elicit more dramatic vasodilation of the limbs in women and that this might be explained by reduced MSNA reactivity and/or blunted sympathetic vascular transduction. We measured heart rate (HR), mean arterial pressure (MAP), CBF, calf vascular conductance (CVC), forearm blood flow (FBF), forearm vascular conductance (FVC), and MSNA concurrently in 18 men (age: 23 ± 2 yr) and 16 women (age: 24 ± 2 yr) during 5 min of supine baseline and 5 min of mental stress. Mental stress elicited similar increases in MAP (Δ10 ± 1 vs. Δ11 ± 1 mmHg), HR (Δ16 ± 2 vs. Δ17 ± 2 beats/min), FBF (Δ81 ± 16% vs. Δ83 ± 15%), and FVC (Δ62 ± 13% vs. Δ65 ± 13%) in men and women, respectively. In contrast, CBF (Δ16 ± 8% vs. Δ37 ± 9%, P = 0.036) and CVC (Δ4 ± 7% vs. Δ24 ± 8%, P = 0.036) responses were exaggerated in women compared with men. Changes in FVC were significantly correlated with changes in CVC in women ( r = 0.681, P = 0.004) but not in men. MSNA reactivity to mental stress was not different between men and women; however, changes in CVC were negatively correlated with increases of MSNA in men ( r = −0.411, P = 0.045) but not in women. In conclusion, our data suggest different patterns of calf vascular reactivity to mental stress in men and women that might relate, in part, to altered vascular transduction of MSNA.

scholarly journals Combined heat and mental stress alters neurovascular control in humans

2010 ◽  
Vol 109 (6) ◽  
pp. 1880-1886 ◽  
Author(s):  
Jenna C. Klein ◽  
Craig G. Crandall ◽  
R. Matthew Brothers ◽  
Jason R. Carter
Keyword(s):  
Heart Rate ◽  
Heat Stress ◽  
Mental Stress ◽  
Muscle Sympathetic Nerve Activity ◽  
Thermal Conditions ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Vascular Responses ◽  
Time Condition ◽  
Forearm Skin

This study examined the effect of combined heat and mental stress on neurovascular control. We hypothesized that muscle sympathetic nerve activity (MSNA) and forearm vascular responses to mental stress would be augmented during heat stress. Thirteen subjects performed 5 min of mental stress during normothermia (Tcore; 37 ± 0°C) and heat stress (38 ± 0°C). Heart rate, mean arterial pressure (MAP), MSNA, forearm vascular conductance (FVC; venous occlusion plethysmography), and forearm skin vascular conductance (SkVCf; via laser-Doppler) were analyzed. Heat stress increased heart rate, MSNA, SkVCf, and FVC at rest but did not change MAP. Mental stress increased MSNA and MAP during both thermal conditions; however, the increase in MAP during heat stress was blunted, whereas the increase in MSNA was accentuated, compared with normothermia (time × condition; P < 0.05 for both). Mental stress decreased SkVCf during heat stress but not during normothermia (time × condition, P < 0.01). Mental stress elicited similar increases in heart rate and FVC during both conditions. In one subject combined heat and mental stress induced presyncope coupled with atypical blood pressure and cutaneous vascular responses. In conclusion, these findings indicate that mental stress elicits a blunted increase of MAP during heat stress, despite greater increases in total MSNA and cutaneous vasoconstriction. The neurovascular responses to combined heat and mental stress may be clinically relevant to individuals frequently exposed to mentally demanding tasks in hyperthermic environmental conditions (i.e., soldiers, firefighters, and athletes).

scholarly journals Habitual cigarette smoking raises pressor responses to spontaneous bursts of muscle sympathetic nerve activity

2019 ◽  
Vol 317 (2) ◽  
pp. R280-R288 ◽  
Author(s):  
Jian Cui ◽  
Rachel C. Drew ◽  
Matthew D. Muller ◽  
Cheryl Blaha ◽  
Virginia Gonzalez ◽  
...  
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Total Activity ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Pressor Responses ◽  
Averaging Techniques

Smoking is a risk factor for cardiovascular diseases. Prior reports showed a transient increase in blood pressure (BP) following a spontaneous burst of muscle sympathetic nerve activity (MSNA). We hypothesized that this pressor response would be accentuated in smokers. Using signal-averaging techniques, we examined the BP (Finometer) response to MSNA in 18 otherwise healthy smokers and 42 healthy nonsmokers during resting conditions. The sensitivities of baroreflex control of MSNA and heart rate were also assessed. The mean resting MSNA, heart rate, and mean arterial pressure (MAP) were higher in smokers than nonsmokers. The MAP increase following a burst of MSNA was significantly greater in smokers than nonsmokers (Δ3.4 ± 0.3 vs. Δ1.6 ± 0.1 mmHg, P < 0.001). The baroreflex sensitivity (BRS) of burst incidence, burst area, or total activity was not different between the two groups. However, cardiac BRS was lower in smokers than nonsmokers (14.6 ± 1.7 vs. 24.6 ± 1.5 ms/mmHg, P < 0.001). Moreover, the MAP increase following a burst was negatively correlated with the cardiac BRS. These observations suggest that habitual smoking in otherwise healthy individuals raises the MAP increase following spontaneous MSNA and that the attenuated cardiac BRS in the smokers was a contributing factor. We speculate that the accentuated pressor increase in response to spontaneous MSNA may contribute to the elevated resting BP in the smokers.

Forearm neurovascular responses during mental stress and vestibular activation

2005 ◽  
Vol 288 (2) ◽  
pp. H904-H907 ◽  
Author(s):  
Jason R. Carter ◽  
William H. Cooke ◽  
Chester A. Ray
Keyword(s):  
Mental Stress ◽  
Sympathetic Nerve Activity ◽  
Forearm Blood Flow ◽  
Mental Arithmetic ◽  
Muscle Sympathetic Nerve Activity ◽  
Vestibular Stimulation ◽  
Nerve Activity ◽  
Vestibulosympathetic Reflex ◽  
Unexplained Syncope ◽  
Forearm Vascular Resistance

Autonomic responses may underlie associations among anxiety, vestibular dysfunction, and unexplained syncope. Mental stress (MS), an anxiety-inducing stimulus, causes forearm vasodilation, whereas the vestibulosympathetic reflex (VSR) causes forearm vasoconstriction. The purpose of this study was to examine the combined effects of mental and vestibular stimulation on neurovascular control in the forearm. Heart rate, arterial pressure (Finapres), and forearm blood flow (Doppler) were measured in 10 healthy volunteers in the prone position during 1) head-down rotation (HDR), 2) MS (mental arithmetic), and 3) HDR + MS. Forearm vascular resistance (FVR) increased during HDR (from 232 ± 40 to 319 ± 53 units) and decreased during MS (from 260 ± 57 to 154 ± 22 units). During HDR + MS, FVR did not change [change (Δ) = −31 ± 50 units] and was not significantly different from the algebraic sum of each trial performed alone (Δ = −20 ± 42 units). Arm muscle sympathetic nerve activity (MSNA; microneurography) was measured in seven additional subjects. MSNA increased during HDR (from 13 ± 2 to 17 ± 2 bursts/min) and HDR + MS (from 11 ± 2 to 16 ± 2 bursts/min). Increases in MSNA during HDR + MS (Δ = 5 ± 2 bursts/min) were not different from the algebraic sum of each trial performed alone (Δ = 6 ± 2 bursts/min). We conclude that an additive neurovascular interaction exists between MS and the VSR in the forearm. Activation of the VSR prevented forearm vasodilation during MS, suggesting that activation of the VSR may help protect against stress-induced syncope.

scholarly journals Attenuation of sympathetic baroreflex sensitivity during the onset of acute mental stress in humans

2011 ◽  
Vol 300 (5) ◽  
pp. H1788-H1793 ◽  
Author(s):  
John J. Durocher ◽  
Jenna C. Klein ◽  
Jason R. Carter
Keyword(s):  
Arterial Pressure ◽  
Strong Correlation ◽  
Mental Stress ◽  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Cardiac Cycle ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Spontaneous Fluctuations

Mental stress consistently induces a pressor response that is often accompanied by a paradoxical increase of muscle sympathetic nerve activity (MSNA). The purpose of the present study was to evaluate sympathetic baroreflex sensitivity (BRS) by examining the relations between spontaneous fluctuations of diastolic arterial pressure (DAP) and MSNA. We hypothesized that sympathetic BRS would be attenuated during mental stress. DAP and MSNA were recorded during 5 min of supine baseline, 5 min of mental stress, and 5 min of recovery in 32 young healthy adults. Burst incidence and area were determined for each cardiac cycle and placed into 3-mmHg DAP bins; the slopes between DAP and MSNA provided an index of sympathetic BRS. Correlations between DAP and MSNA were strong (>0.5) during baseline in 31 of 32 subjects, but we evaluated the change in slope only for those subjects maintaining a strong correlation during mental stress (16 subjects). During baseline, the relation between DAP and MSNA was negative when expressed as either burst incidence [slope = −1.95 ± 0.18 bursts·(100 beats)−1·mmHg−1; r = −0.86 ± 0.03] or total MSNA [slope = −438 ± 91 units·(beat)−1 mmHg−1; r = −0.76 ± 0.06]. During mental stress, the slope between burst incidence and DAP was significantly reduced [slope = −1.14 ± 0.12 bursts·(100 beats)−1·mmHg−1; r = −0.72 ± 0.03; P < 0.01], indicating attenuation of sympathetic BRS. A more detailed analysis revealed an attenuation of sympathetic BRS during the first 2 min of mental stress ( P < 0.01) but no change during the final 3 min of mental stress ( P = 0.25). The present study demonstrates that acute mental stress attenuates sympathetic BRS, which may partially contribute to sympathoexcitation during the mental stress-pressor response. However, this attenuation appears to be isolated to the onset of mental stress. Moreover, variable MSNA responses to mental stress do not appear to be directly related to sympathetic BRS.

scholarly journals Sympathetic neural responses to mental stress: responders, nonresponders and sex differences

2009 ◽  
Vol 296 (3) ◽  
pp. H847-H853 ◽  
Author(s):  
Jason R. Carter ◽  
Chester A. Ray
Keyword(s):  
Perceived Stress ◽  
Mental Stress ◽  
Sympathetic Nerve Activity ◽  
Mental Arithmetic ◽  
Muscle Sympathetic Nerve Activity ◽  
Neural Responses ◽  
Nerve Activity ◽  
Women Subjects ◽  
Stress Levels ◽  
Vascular Responsiveness

Mental stress consistently increases heart rate (HR) and blood pressure (BP) in humans, despite inconsistent sympathetic neural responses that include increases, decreases, or no change in muscle sympathetic nerve activity (MSNA). The purpose of the present study was to examine associations between MSNA, BP, and HR responses to mental stress. Leg MSNA, BP, HR, and perceived stress levels were recorded during 3–5 min of mental arithmetic in 82 subjects (53 men and 29 women). Subjects were divided into positive responders (≥Δ3 bursts/min; n = 40), negative responders (≤Δ−3 bursts/min; n = 9), and nonresponders ( n = 33). Mental stress increased MSNA in positive responders (Δ6 ± 1 bursts/min), decreased MSNA in negative responders (Δ−6 ± 1 bursts/min), and did not change MSNA in nonresponders (Δ1 ± 1 bursts/min). Mental stress increased mean BP and HR similarly in positive responders (Δ15 ± 1 mmHg and Δ16 ± 1 beats/min; P < 0.001), nonresponders (Δ15 ± 1 mmHg and Δ19 ± 2 beats/min; P < 0.001), and negative responders (Δ12 ± 2 mmHg and Δ19 ± 3 beats/min; P < 0.001). Perceived stress levels and sex distributions were similar across responders and nonresponders; thus, perceived stress and sex do not appear to influence MSNA during mental stress. However, men demonstrated higher increases of mean BP during mental stress when compared with women (Δ16 ± 1 vs. Δ12 ± 1 mmHg; P < 0.05), despite no differences in MSNA responses. In conclusion, our results demonstrate marked differences in MSNA responses to mental stress and a disassociation between MSNA and BP responses to mental stress, suggesting complex patterns of vascular responsiveness during mental stress.

scholarly journals Sympathetic neural reactivity to mental stress differs in black and non-Hispanic white adults

2018 ◽  
Vol 124 (1) ◽  
pp. 201-207 ◽  
Author(s):  
Ida T. Fonkoue ◽  
Christopher E. Schwartz ◽  
Min Wang ◽  
Jason R. Carter
Keyword(s):  
Heart Rate ◽  
Black Men ◽  
Sympathetic Nerve ◽  
Mental Stress ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Black Adults ◽  
Nerve Activity ◽  
Neural Reactivity ◽  
Hispanic White

Black adults have a higher risk of hypertension compared with non-Hispanic white (NHW) adults, but physiological mechanisms underlying this predisposition remain unclear. This study compared muscle sympathetic nerve activity (MSNA) responses to mental stress in a group of young black and NHW participants. We hypothesized that the sympathoexcitation associated with mental stress would be greater in black adults compared with NHW participants. Thirty-five male adults (19 black, 23 ± 1 yr; 16 NHW, 22 ± 1 yr) were examined during 5-min supine baseline and 5 min of mental stress (via mental arithmetic). Baseline mean arterial pressure (80 ± 2 vs. 82 ± 1 mmHg), heart rate (61 ± 4 vs. 61 ± 2 beats/min), MSNA (13 ± 1 vs. 15 ± 2 bursts/min), and sympathetic baroreflex sensitivity (−1.1 ± 0.4 vs. −1.5 ± 0.3 bursts·100 heart beats−1·mmHg−1) were not significantly different between NHW and black adults ( P > 0.05), respectively. MSNA reactivity to mental stress was significantly higher in NHW compared with black adults (time × race, P = 0.006), with a particularly divergent responsiveness during the first minute of mental stress in NHW (Δ4 ± 1 burst/min) and black (Δ−2 ± 2 burst/min; P = 0.022) men. Blood pressure and heart rate reactivity to mental stress were similar between groups. In summary, black participants demonstrated a lower MSNA responsiveness to mental stress compared with NHW adults. These findings suggest that, despite a higher prevalence of hypertension, black subjects do not appear to have higher neural and cardiovascular responsiveness to mental stress compared with NHW. NEW & NOTEWORTHY Black men have a blunted muscle sympathetic nerve activity response to mental stress compared with non-Hispanic white (NHW) men, especially at the onset of mental stress when muscle sympathetic nerve activity decreased in blacks and increased in NHW men. Thus, despite a high prevalence of hypertension in blacks, normotensive NHW men display a greater peripheral sympathetic neural reactivity to mental stress than black men.

scholarly journals Otolithic activation on visceral circulation in humans: effect of aging

2008 ◽  
Vol 295 (4) ◽  
pp. F1166-F1169 ◽  
Author(s):  
Charity L. Sauder ◽  
Erin E. Conboy ◽  
Stephanie A. Chin-Sang ◽  
Chester A. Ray
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve Activity ◽  
Blood Velocity ◽  
Otolith Organs ◽  
Otolith Organ ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Vascular Responses ◽  
Arterial Blood ◽  
Older Subjects

Engagement of the otolith organs elicits differential activation of sympathetic nerve activity and vascular responses to muscle and skin in humans. Additionally, aging attenuates the otolith organ-mediated increases in muscle sympathetic nerve activity in older adults. In this study, we hypothesized that 1) the vestibulosympathetic reflex (VSR) would elicit visceral vascular vasoconstriction and 2) visceral vascular response to the VSR would be attenuated in older subjects compared with young. To test these hypotheses, heart rate, mean arterial blood pressure, and renal, celiac trunk, and superior mesenteric arterial blood velocity (Doppler ultrasound) were measured in 22 young (25 ± 1 yr) and 18 older (65 ± 2 yr) healthy subjects during head-down rotation (HDR), which selectively activates the otolith organs. Mean arterial pressure and heart rate did not change from baseline during HDR in young or older subjects. Renal blood velocity (Δ −2 ± 1 cm/s) and vascular conductance (Δ −0.03 ± 0.01 cm·s−1·mmHg−1) significantly decreased from baseline during HDR ( P < 0.05) in young subjects. In contrast, renal blood velocity and conductance did not change in older subjects (Δ −0.2 ± 1 cm/s and Δ0.02 ± 0.08 mmHg·cm−1·s−1, respectively) during HDR. Superior mesenteric and celiac blood velocity and vascular conductance did not change in response to HDR in either the young or older subjects. These data suggest that renal vasoconstriction occurs during otolith organ activation in young but not older humans. Together with our previous studies, we conclude that the VSR elicits a diverse patterning of sympathetic outflow that results in heterogeneous vascular responses in humans and that these responses are significantly attenuated in older humans.

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