scholarly journals Influence of age and sex on the pressor response following a spontaneous burst of muscle sympathetic nerve activity

2012 ◽  
Vol 302 (11) ◽  
pp. H2419-H2427 ◽  
Author(s):  
Lauro C. Vianna ◽  
Emma C. Hart ◽  
Seth T. Fairfax ◽  
Nisha Charkoudian ◽  
Michael J. Joyner ◽  
...  
Keyword(s):  
Postmenopausal Women ◽  
Sympathetic Nerve ◽  
Healthy Aging ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Older Men ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Age And Sex

The sympathetic nervous system is critical for the beat-to-beat regulation of arterial blood pressure (BP). Although studies have examined age- and sex-related effects on BP control, findings are inconsistent and limited data are available in postmenopausal women. In addition, the majority of studies have focused on time-averaged responses without consideration for potential beat-to-beat alterations. Thus we examined whether the ability of muscle sympathetic nerve activity (MSNA) to modulate BP on a beat-to-beat basis is affected by age or sex. BP and MSNA were measured during supine rest in 40 young (20 men) and 40 older (20 men) healthy subjects. Beat-to-beat fluctuations in mean arterial pressure (MAP) were characterized for 15 cardiac cycles after each MSNA burst using signal averaging. The rise in MAP following an MSNA burst was similar between young men and women (+2.64 ± 0.3 vs. +2.57 ± 0.3 mmHg, respectively). However, the magnitude of the increase in MAP after an MSNA burst was reduced in older compared with young subjects ( P < 0.05). Moreover, the attenuation of the pressor response was greater in older women (+1.20 ± 0.1 mmHg) compared with older men (+1.72 ± 0.2 mmHg; P < 0.05). Interestingly, in all groups, MAP consistently decreased after cardiac cycles without MSNA bursts (nonbursts) with the magnitude of fall greatest in older men. In summary, healthy aging is associated with an attenuated beat-to-beat increase in BP after a spontaneous MSNA burst, and this attenuation is more pronounced in postmenopausal women. Furthermore, our nonburst findings highlight the importance of sympathetic vasoconstrictor activity to maintain beat-to-beat BP, particularly in older men.

scholarly journals Spontaneous bursts of muscle sympathetic nerve activity decrease leg vascular conductance in resting humans

2013 ◽  
Vol 304 (5) ◽  
pp. H759-H766 ◽  
Author(s):  
Seth T. Fairfax ◽  
Jaume Padilla ◽  
Lauro C. Vianna ◽  
Michael J. Davis ◽  
Paul J. Fadel
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Burst Size ◽  
Muscle Sympathetic Nerve Activity ◽  
Common Femoral Artery ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Arterial Blood

Previous studies in humans attempting to assess sympathetic vascular transduction have related large reflex-mediated increases in muscle sympathetic nerve activity (MSNA) to associated changes in limb vascular resistance. However, such procedures do not provide insight into the ability of MSNA to dynamically control vascular tone on a beat-by-beat basis. Thus we examined the influence of spontaneous MSNA bursts on leg vascular conductance (LVC) and how variations in MSNA burst pattern (single vs. multiple bursts) and burst size may affect the magnitude of the LVC response. In 11 young men, arterial blood pressure, common femoral artery blood flow, and MSNA were continuously recorded during 20 min of supine rest. Signal averaging was used to characterize percent changes in LVC for 15 cardiac cycles following heartbeats associated with and without MSNA bursts. LVC significantly decreased following MSNA bursts, reaching a nadir during the 6th cardiac cycle (single bursts, −2.9 ± 1.1%; and multiple bursts, −11.0 ± 1.4%; both, P < 0.001). Individual MSNA burst amplitudes and the total amplitude of consecutive bursts were related to the magnitude of peak decreases in LVC. In contrast, cardiac cycles without MSNA bursts were associated with a significant increase in LVC (+3.1 ± 0.5%; P < 0.001). Total vascular conductance decreased in parallel with LVC also reaching a nadir around the peak rise in arterial blood pressure following an MSNA burst. Collectively, these data are the first to assess beat-by-beat sympathetic vascular transduction in resting humans, demonstrating robust and dynamic decreases in LVC following MSNA bursts, an effect that was absent for cardiac cycles without MSNA bursts.

Cardiopulmonary baroreceptor control of muscle sympathetic nerve activity in heat-stressed humans

1999 ◽  
Vol 277 (6) ◽  
pp. H2348-H2352 ◽  
Author(s):  
C. G. Crandall ◽  
R. A. Etzel ◽  
D. B. Farr
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Whole Body ◽  
Nerve Activity ◽  
Arterial Blood

Whole body heating decreases central venous pressure (CVP) while increasing muscle sympathetic nerve activity (MSNA). In normothermia, similar decreases in CVP elevate MSNA, presumably via cardiopulmonary baroreceptor unloading. The purpose of this project was to identify whether increases in MSNA during whole body heating could be attributed to cardiopulmonary baroreceptor unloading coincident with the thermal challenge. Seven subjects were exposed to whole body heating while sublingual temperature, skin blood flow, heart rate, arterial blood pressure, and MSNA were monitored. During the heat stress, 15 ml/kg warmed saline was infused intravenously over 7–10 min to increase CVP and load the cardiopulmonary baroreceptors. We reported previously that this amount of saline was sufficient to return CVP to pre-heat stress levels. Whole body heating increased MSNA from 25 ± 3 to 39 ± 3 bursts/min ( P < 0.05). Central blood volume expansion via rapid saline infusion did not significantly decrease MSNA (44 ± 4 bursts/min, P > 0.05 relative to heat stress period) and did not alter mean arterial blood pressure (MAP) or pulse pressure. To identify whether arterial baroreceptor loading decreases MSNA during heat stress, in a separate protocol MAP was elevated via steady-state infusion of phenylephrine during whole body heating. Increasing MAP from 82 ± 3 to 93 ± 4 mmHg ( P < 0.05) caused MSNA to decrease from 36 ± 3 to 15 ± 4 bursts/min ( P < 0.05). These data suggest that cardiopulmonary baroreceptor unloading during passive heating is not the primary mechanism resulting in elevations in MSNA. Moreover, arterial baroreceptors remain capable of modulating MSNA during heat stress.

Arterial pressure and muscle sympathetic nerve activity are increased after two hours of sustained but not cyclic hypoxia in healthy humans

2005 ◽  
Vol 98 (1) ◽  
pp. 343-349 ◽  
Author(s):  
Renaud Tamisier ◽  
Amit Anand ◽  
Luz M. Nieto ◽  
David Cunnington ◽  
J. Woodrow Weiss
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Oxygen ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Sustained Hypoxia

Sustained and episodic hypoxic exposures lead, by two different mechanisms, to an increase in ventilation after the exposure is terminated. Our aim was to investigate whether the pattern of hypoxia, cyclic or sustained, influences sympathetic activity and hemodynamics in the postexposure period. We measured sympathetic activity (peroneal microneurography), hemodynamics [plethysmographic forearm blood flow (FBF), arterial pressure, heart rate], and peripheral chemosensitivity in normal volunteers on two occasions during and after 2 h of either exposure. By design, mean arterial oxygen saturation was lower during sustained relative to cyclic hypoxia. Baseline to recovery muscle sympathetic nerve activity and blood pressure went from 15.7 ± 1.2 to 22.6 ± 1.9 bursts/min ( P < 0.01) and from 85.6 ± 3.2 to 96.1 ± 3.3 mmHg ( P < 0.05) after sustained hypoxia, respectively, but did not exhibit significant change from 13.6 ± 1.5 to 17.3 ± 2.5 bursts/min and 84.9 ± 2.8 to 89.8 ± 2.5 mmHg after cyclic hypoxia. A significant increase in FBF occurred after sustained, but not cyclic, hypoxia, from 2.3 ± 0.2 to 3.29 ± 0.4 and from 2.2 ± 0.1 to 3.1 ± 0.5 ml·min−1·100 g of tissue−1, respectively. Neither exposure altered the ventilatory response to progressive isocapnic hypoxia. Two hours of sustained hypoxia increased not only muscle sympathetic nerve activity but also arterial blood pressure. In contrast, cyclic hypoxia produced slight but not significant changes in hemodynamics and sympathetic activity. These findings suggest the cardiovascular response to acute hypoxia may depend on the intensity, rather than the pattern, of the hypoxic exposure.

Does infusion of ANG II increase muscle sympathetic nerve activity in patients with primary aldosteronism?

2008 ◽  
Vol 294 (6) ◽  
pp. R1873-R1879 ◽  
Author(s):  
Toshiyoshi Matsukawa ◽  
Takenori Miyamoto
Keyword(s):  
Primary Aldosteronism ◽  
Sympathetic Nerve ◽  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Ang Ii ◽  
Nerve Activity ◽  
Unilateral Adrenalectomy

Patients with primary aldosteronism (PA) were shown to have suppressed muscle sympathetic nerve activity (MSNA) in our previous study. Although baroreflex inhibition probably accounts in part for this reduced MSNA in PA, we hypothesized that the lowered activity of the renin-angiotensin system in PA may also contribute to the suppressed SNA. We recorded MSNA in 9 PA and 16 age-matched normotensive controls (NC). In PA, the resting mean blood pressure (MBP) and serum sodium concentrations were increased, and MSNA was reduced. We examined the effects of infusion of a high physiological dose of ANG II (5.0 ng·kg−1·min−1) on MSNA in 6 of 9 PA and 9 of 16 NC. Infusion of ANG II caused a greater pressor response in PA than NC, but, in spite of the greater increase in pressure, MSNA increased in PA, whereas it decreased in NC. Simultaneous infusion of nitroprusside and ANG II, to maintain central venous pressure at the baseline level and reduce the elevation in MBP induced by ANG II, caused significantly greater increases in MSNA in PA than in NC. Baroreflex sensitivity of heart rate, estimated during phenylephrine infusions, was reduced in PA, but baroreflex sensitivity of MSNA was unchanged in PA compared with NC. All the abnormalities in PA were eliminated following unilateral adrenalectomy. In conclusion, the suppressed SNA in PA depends in part on the low level of ANG II in these patients.

Diazepam reduces both arterial blood pressure and muscle sympathetic nerve activity in human

2004 ◽  
Vol 355 (1-2) ◽  
pp. 77-80 ◽  
Author(s):  
Tsuyoshi Kitajima ◽  
Takashi Kanbayashi ◽  
Yasushi Saito ◽  
Yuji Takahashi ◽  
Yuriko Ogawa ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Arterial Blood

scholarly journals Sexual Dimorphism in Counterregulatory Responses to Hypoglycemia after Antecedent Exercise

2001 ◽  
Vol 86 (8) ◽  
pp. 3516-3524 ◽  
Author(s):  
Pietro Galassetti ◽  
Anthony R. Neill ◽  
Donna Tate ◽  
Andrew C. Ertl ◽  
David H. Wasserman ◽  
...  
Keyword(s):  
Sexual Dimorphism ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Glucose Production ◽  
Cardiovascular Responses ◽  
Endogenous Glucose Production ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Blood Pressures

After antecedent hypoglycemia, counterregulatory responses to subsequent hypoglycemia exhibit greater blunting in men than in women. Because physical exercise and hypoglycemia share multiple counterregulatory mechanisms, we hypothesized that prior exercise may also result in gender-specific blunting of counterregulatory responses to subsequent hypoglycemia. Thirty healthy subjects (15 women and 15 men; age, 28 ± 3 yr; body mass index, 23 ± 1 kg/m2) were studied during 2-d experiments. Day 1 consisted of either identical 90-min morning and afternoon cycle exercise at 50% maximum oxygen expenditure or two 2-h episodes of hyperinsulinemic euglycemia. Day 2 consisted of a 2-h morning hyperinsulinemic-hypoglycemic clamp. Endogenous glucose production was measured using [3-3H]glucose. Muscle sympathetic nerve activity was measured using microneurography. Day 2 insulin (540± 36 pmol/liter) and plasma glucose (2.9 ± 0.06 pmol/liter) levels were similar in men and women during the last 30 min of hypoglycemia. Compared with antecedent euglycemia, d 1 exercise produced significant blunting of d 2 counterregulatory responses to hypoglycemia. Several key d 2 counterregulatory responses were blunted to a greater extent in men than in women: glucagon (men, −105 ± 14; women, −25 ± 7 ng/liter; P &lt; 0.0001), epinephrine (men, −2625 ± 257 pmol/liter; women, −212 ± 573; P &lt; 0.001), norepinephrine (men, −0.50± 0.12 nmol/liter; women, −0 ± 0.11; P &lt; 0.001), and muscle sympathetic nerve activity (men, −13 ± 4; women, −4 ± 4 bursts/min; P &lt; 0.01). Cardiovascular responses (heart rate and systolic and mean arterial blood pressures) were also more blunted by antecedent exercise in men than in women. After d 1 exercise, the amount of glucose infused during d 2 hypoglycemia in men was increased 6-fold compared with that after d 1 euglycemia. This amount was significantly increased (P &lt; 0.01) compared with the 2-fold (P &lt; 0.01) increment in glucose infusion that was required in women after d 1 exercise. Lipolysis was unaffected by d 1 exercise in women, but was significantly blunted during d 2 hypoglycemia in men. In summary, two bouts of prolonged, moderate exercise (90 min at 50% maximum oxygen expenditure) induced a marked sexual dimorphism in key neuroendocrine (glucagon, catecholamines, and muscle sympathetic nerve activity) and metabolic (glucose kinetic, lipolysis) responses to next day hypoglycemia.

Delayed and diminished pressor response to muscle sympathetic nerve activity in the elderly

1996 ◽  
Vol 80 (3) ◽  
pp. 869-875 ◽  
Author(s):  
Y. Sugiyama ◽  
T. Matsukawa ◽  
A. S. Shamsuzzaman ◽  
H. Okada ◽  
T. Watanabe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Pressure Rise ◽  
The Elderly ◽  
Young Group ◽  
Nerve Activity

We studied the effects of aging on alpha-receptor-mediated vasoconstrictive responses to sympathetic nerve activity in 16 healthy aged [75.8 +/- 2.7 (SE) yr] and young men (33.8 +/- 2.0 yr). Muscle sympathetic nerve activity (MSNA), heart rate, and blood pressure were analyzed during slow respiration (0.1 Hz). Peak amplitude and phase were calculated from a cosine function fitted with 0.1 Hz by using the least squares method. The latency of the pressor response to MSNA, defined as lag time from the peak of MSNA to diastolic blood pressure, was significantly longer in the aged than the young group (7.1 +/- 0.3 vs. 5.4 +/- 0.4 s; P < 0.01). The extent of pressor response to MSNA, defined as diastolic blood pressure rise in response to increase in total MSNA, was significantly lower in the aged than the young group (0.038 +/- 0.006 vs. 0.099 +/- 0.024 mmHg/unit, P < 0.001). These results suggest that alpha-receptor-mediated vasoconstrictive responses to MSNA may be attenuated in the elderly.

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.

Abstract 125: Elevated Muscle Sympathetic Nerve Activity is Associated With Higher Aortic and Carotid Stiffness Independent of Blood Pressure in Women

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Seth W Holwerda ◽  
Rachel E Luehrs ◽  
Nealy A Wooldridge ◽  
Lyndsey E DuBose ◽  
Jess G Fiedorowicz ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Strongly Correlated ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Age Related ◽  
Related Increase

Central arterial stiffness, a significant contributor to the development of hypertension and cardiovascular disease with aging, is linked to elevated muscle sympathetic nerve activity (MSNA) in men. However, the extent to which MSNA is associated with central arterial stiffness in women is unknown. Given that the age-related increase in MSNA and arterial blood pressure (BP) occurs at a steeper rate among women compared to men, we tested the hypothesis that resting MSNA is more strongly correlated with central arterial stiffness in women than in men. Also, because of the parallel age-related increase in MSNA, we further hypothesized that the relation between MSNA and central arterial stiffness would not be independent of age. MSNA (microneurography), aortic stiffness (carotid-femoral pulse wave velocity, CFPWV), and carotid β-stiffness (carotid tonometry and ultrasound) were assessed in 54 healthy men (n=29; 19-72 yrs; 30 ± 1 kg/m 2 ; systolic BP: 128 ± 3 mmHg) and women (n=26; 26-64 yrs; 29 ± 2 kg/m 2 ; systolic BP: 116 ± 3 mmHg). No differences between men and women were observed for CFPWV (Men: 7.0 ± 0.3 vs. Women: 6.8 ± 0.4 mmHg, P=0.747) and carotid β-stiffness (Men: 7.6 ± 0.8 vs. Women: 7.6 ± 0.5 mmHg, P=0.975). Mean BP was lower in women compared to men (Men: 93 ± 3 vs. Women: 85 ± 2 mmHg, P=0.021) and MSNA tended to be lower in women compared to men (Men: 25 ± 3 vs. Women: 20 ± 2 bursts/min, P=0.091). After adjusting for mean BP and HR (partial correlation), CFPWV was significantly correlated with MSNA in men (R=0.44, P=0.021) and women (R=0.58, P=0.004). Interestingly, further adjustment for age abolished the association between CFPWV and MSNA in men (R=0.01, P=0.968), but not in women (R=0.43, P=0.046). A moderate relation between carotid β-stiffness and MSNA was observed in men (R=0.37, P=0.063) and women (R=0.44, P=0.034), but was abolished after adjusting for age (Men: R=-0.001, P=0.995; Women: R=0.26, P=0.245). These preliminary data demonstrate that MSNA is positively correlated with central arterial stiffness in women and men independent of BP. Furthermore, abolishment of the relation between MSNA and CFPWV in men only when adjusting for age suggests that the association between MSNA and central arterial stiffness may be more robust in women.

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