Abstract 15287: Muscle Sympathetic Nerve Activity and Arterial Stiffness in Resistant Hypertensive Patients With Metabolic Syndrome

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
C. Tsioufis ◽  
K. Dimitriadis ◽  
E. Koutra ◽  
A. Kasiakogias ◽  
A. Kordalis ◽  
...  

Introduction: Resistant hypertension is related to sympathetic overdrive and arterial stiffening, while there are scarce data whether metabolic syndrome further potentiates sympathetic activity and vascular abnormalities in this setting. Hypothesis: The aim of this study was to assess the effect of the metabolic syndrome on muscle sympathetic nerve activity (MSNA) and arterial stiffness in resistant hypertensive patients. Method: We studied 24 patients with resistant hypertension [age: 58±10 years, 15 males, office blood pressure (BP): 178/94±15/12 mmHg, 24-hour BP: 149/84±15/11 mmHg, under 4.2±0.5 drugs] that underwent transthoracic echocardiographic study and blood sampling for assessment of the metabolic profile. Metabolic syndrome was defined according to the Adult Treatment Panel III criteria and arterial stiffness was evaluated on the basis of carotid to femoral pulse wave velocity (PWV). In all participants sympathetic drive was assessed by MSNA estimations based on established methodology (microneurography). Results: Resistant hypertensive patients with metabolic syndrome (n=11) compared to those without (n=13) exhibited higher waist circumference (108.1±5.4 vs 94.6±9.2 cm, p=0.001), fasting glucose (131.8±2.9 vs 94.6±2.1 mg/dl, p<0.05), office systolic BP (186±17 vs 171±15 mmHg, p<0.001) and left ventricular mass index (134.2±18.1 vs 124.6±17.2 g/m2, p=0.001). Moreover, metabolic syndrome patients compared to those without were characterized by greater levels of carotid to femoral PWV (11.7±0.8 vs 9.3±1.1 m/sec, p<0.001) and sympathetic nerve traffic as reflected by MSNA levels (84.2±2.8 vs 75.1±2.2 bursts per 100 heart beats, p<0.001). In all participants MSNA was related to waist circumference (r=0.38, p=0.002) and office systolic BP levels (r=0.35, p<0.05) but there was no association with PWV values (p=NS). Conclusions: In resistant hypertensive patients, metabolic syndrome is associated with high MSNA and PWV levels. These findings support that metabolic syndrome further deteriorates sympathetic activity and arterial stiffening characterizing resistant hypertension.

2013 ◽  
Vol 26 (7) ◽  
pp. 912-917 ◽  
Author(s):  
S. B. C. de Souza ◽  
J. A. Rocha ◽  
M. A. R. Cuoco ◽  
G. M. Guerra ◽  
J. C. Ferreira-Filho ◽  
...  

2005 ◽  
Vol 98 (1) ◽  
pp. 343-349 ◽  
Author(s):  
Renaud Tamisier ◽  
Amit Anand ◽  
Luz M. Nieto ◽  
David Cunnington ◽  
J. Woodrow Weiss

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.


Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Seth W Holwerda ◽  
Rachel E Luehrs ◽  
Nealy A Wooldridge ◽  
Lyndsey E DuBose ◽  
Jess G Fiedorowicz ◽  
...  

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.


2009 ◽  
Vol 94 (4) ◽  
pp. 1361-1366 ◽  
Author(s):  
Dileep V. Menon ◽  
Debbie Arbique ◽  
Zhongyun Wang ◽  
Beverley Adams-Huet ◽  
Richard J. Auchus ◽  
...  

2000 ◽  
Vol 85 (9) ◽  
pp. 3203-3207 ◽  
Author(s):  
Brunella Capaldo ◽  
Giuseppe Lembo ◽  
Virgilio Rendina ◽  
Raffaele Guida ◽  
Paolo Marzullo ◽  
...  

Abstract Muscle sympathetic nerve activity was measured in nine acromegalic patients (age, 35 ± 4 yr; body mass index, 28 ± 2 kg/m2) and eight healthy subjects (age, 32 ± 3 yr; body mass index, 25 ± 2 kg/m2) by combining the forearm arterial-venous difference technique with the tracer method[ infusion of tritiated norepinephrine (NE)]. Muscle NE release was quantified both at rest and during physiological hyperinsulinemia while maintaining euglycemia (∼90 mg/dL) by means of the euglycemic clamp. Arterial plasma NE was similar in the two groups at rest (197 ± 28 and 200 ± 27 pg/mL−1) and slightly increased during insulin infusion. Forearm NE release was 2.33 ± 0.55 ng·liter−1·min−1 in healthy subjects and 2.67 ± 0.61 ng·liter−1·min−1 in acromegalic subjects in the basal state and increased to a similar extent during insulin infusion in both groups (3.13 ± 0.71 and 3.32 ± 0.75 ng·L−1· min−1, P &lt; 0.05 vs. basal), indicating a normal stimulatory effect of insulin on muscle sympathetic activity. In contrast, insulin-stimulated forearm glucose uptake was markedly lower in acromegalic patients (2.3 ± 0.4 mg·L−1·min−1) than in control subjects (7.9 ± 1.3 mg·L−1·min−1, P &lt; 0.001), indicating the presence of severe insulin resistance involving glucose metabolism. Our data demonstrate that patients with long-term acromegaly have normal sympathetic activity in the skeletal muscle in the basal, postabsorptive state and normal increments in NE spillover in response to the sympatho-excitatory effect of insulin. Thus, the presence of severe insulin resistance in acromegaly is not accounted for by adrenergic mechanisms.


2002 ◽  
Vol 93 (3) ◽  
pp. 857-864 ◽  
Author(s):  
John R. Halliwill ◽  
Christopher T. Minson

We tested the hypothesis that acute hypoxia would alter the sensitivity of arterial baroreflex control of both heart rate and sympathetic vasoconstrictor outflow. In 16 healthy, nonsmoking, normotensive subjects (8 women, 8 men, age 20–33 yr), we assessed baroreflex control of heart rate and muscle sympathetic nerve activity by using the modified Oxford technique during both normoxia and hypoxia (12% O2). Compared with normoxia, hypoxia reduced arterial O2 saturation levels from 96.8 ± 0.3 to 80.7 ± 1.4% ( P < 0.001), increased heart rate from 59.8 ± 2.4 to 79.4 ± 2.9 beats/min ( P < 0.001), increased mean arterial pressure from 96.7 ± 2.5 to 105.0 ± 3.3 mmHg ( P = 0.002), and increased sympathetic activity 126 ± 58% ( P < 0.05). The sensitivity for baroreflex control of both heart rate and sympathetic activity was not altered by hypoxia (heart rate: −1.02 ± 0.09 vs. −1.02 ± 0.11 beats · min−1 · mmHg−1; nerve activity: −5.6 ± 0.9 vs. −6.2 ± 0.9 integrated activity · beat−1 · mmHg−1; both P > 0.05). Acute exposure to hypoxia reset baroreflex control of both heart rate and sympathetic activity to higher pressures without changes in baroreflex sensitivity.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
H Sugimoto ◽  
H Murai ◽  
T Hamaoka ◽  
Y Mukai ◽  
O Inoue ◽  
...  

Abstract Background Arterial reflected wave is determined by not only atherosclerosis but also sympathetic nerve activity. Recently, Arterial Velocity pulse Index (AVI), which is an index of arterial reflected waves, and Arterial Pressure volume Index (API), which is an index of volume of a conductive blood vessel, have been proposed as new index of arterial stiffness. However, it is unclear whether API and AVI would be associated with muscle sympathetic nerve activity (MSNA) in hypertensive subjects. Purpose The purpose of this study was to evaluate the correlation between AVI, API and MSNA in hypertensive subjects. Method 41 hypertensive patients and 40 non-hypertensive subjects were included in this study. We performed a cross-sectional, observational study. Hypertension (HT) was defined as systolic blood pressure (SBP) ≥140 mmHg, diastolic blood pressure (DBP) ≥90 mmHg or medical treatment for HT. AVI and API was measured by NAS-1000 (Nihon Koden, Japan). MSNA, central sympathetic outflow to peripheral muscle, was recorded directly from peroneal nerve. MSNA was expressed by burst frequency (bursts/minute) and burst incidence (bursts/100heartbeats). Blood pressure, heart rate and MSNA were recorded simultaneously. Results Age, systolic and diastolic pressure were significantly higher in hypertensive patients compared to control (40±15 vs 61±13 years, p&lt;0.001; 142±16 vs 113±9 mmHg, p&lt;0.001; 81±14 vs 67±9 mmHg, p&lt;0.001). MSNA and AVI were significantly augmented in hypertensive patients compared to control (34±11 vs. 23±6 bursts/min, p&lt;0.05; 26±7 vs. 16±4, p&lt;0.05). AVI was correlated with MSNA in each group (hypertension: r=0.59, P&lt;0.001, non-hypertension: r=0.51, p&lt;0.001). However, no correlation was shown between API and MSNA in each group (hypertension: r=0.22, p=0.15, non-hypertension: r=0.07, p=0.63). Multiple regression analysis also showed MSNA was significantly related with AVI but was not with API. Conclusion Our finding showed that AVI relates to MSNA independent of API in patients with hypertension. It suggested that Novel index of arterial reflected waves, AVI, is helpful to estimate augmented SNA in hypertensive subjects regardless of volume of a conductive blood vessel. Funding Acknowledgement Type of funding source: None


2014 ◽  
Vol 176 (1) ◽  
pp. 8-12 ◽  
Author(s):  
E.E. Vink ◽  
W.L. Verloop ◽  
L. Siddiqi ◽  
L.J. van Schelven ◽  
P. Liam Oey ◽  
...  

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