Baroreflex Sensitivity in Obesity: Relationship With Cardiac Autonomic Nervous System Activity

Skrapari, Ioanna; Tentolouris, Nicholas; Περρέα, Δέσποινα; Bakoyiannis, Christos; Papazafiropoulou, Athanasia; Katsilambros, Nicholas

doi:10.1038/oby.2007.201

Cited by 127 publications

(110 citation statements)

References 47 publications

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“…Previous studies observed an association between BMI and sympathetic activation (1,2,29). However, BMI may not be a valid measure to describe body composition because it does not distinguish between body fat and lean body mass.…”

Section: Tablementioning

confidence: 99%

Body fat, especially visceral fat, is associated with electrocardiographic measures of sympathetic activation

Hillebrand

Mutsert

Christen

et al. 2014

Obesity

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Objective: Obesity is associated with sympathetic activation, but the role of different fat depots is unclear. The association between body fat, specifically visceral fat, and electrocardiographic measures of sympathetic activation in a population with structurally normal hearts was investigated. Methods: In this cross-sectional baseline analysis of the Netherlands Epidemiology of Obesity study, body fat percentage was assessed with BIA and abdominal subcutaneous (SAT) and visceral adipose tissue (VAT) with magnetic resonance (MR) imaging. Mean heart rate (HR) and five other electrocardiographic measures of sympathetic activation were calculated. We performed multivariate linear regression analyses. Results: In 868 participants with a mean age(SD) of 55(6) years, BMI of 26(4) kg/m 2 , 47% men, body fat was associated with HR and two other measures of sympathetic activation. Per sex-specific SD total body fat, the difference in HR was 1.9 beats/min (95% CI: 1.0, 2.9; P < 0.001) and per SD waist circumference 2.1 beats/min (95% CI: 1.3, 2.9; P < 0.001). The difference in HR per SD VAT was 2.1 beats/min (95% CI: 1.3, 3.0; P < 0.001). Conclusions: Body fat, especially visceral fat, was associated with electrocardiographic measures of sympathetic activation. Our study implies that already before the onset of cardiovascular disease, excess (visceral) body fat is associated with sympathetic activation.

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Section: Tablementioning

confidence: 99%

Body fat, especially visceral fat, is associated with electrocardiographic measures of sympathetic activation

Hillebrand

Mutsert

Christen

et al. 2014

Obesity

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“…The depression of baroreceptor reflex sensitivity during weight gain in humans (4,21) is replicated in animal models of obesity (9,24,25,39,40). Furthermore, the restoration of baroreflex function with weight loss suggests a dynamic interrelationship between diet, metabolic status, and cardiovascular autonomic control (4,21,41,42). Obesity not only increases sympathetic outflow (SNS) to muscle (1,21) and kidneys (45), but it also decreases cardiac parasympathetic (PNS) drive (6,36).…”

mentioning

confidence: 99%

Diet-induced obesity severely impairs myelinated aortic baroreceptor reflex responses

McCully

Brooks

Andresen

2012

American Journal of Physiology-Heart and Circulatory Physiology

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McCully BH, Brooks VL, Andresen MC. Diet-induced obesity severely impairs myelinated aortic baroreceptor reflex responses. Am J Physiol Heart Circ Physiol 302: H2083-H2091, 2012. First published March 9, 2012; doi:10.1152/ajpheart.01200.2011.-Diet-induced obesity (DIO) attenuates the arterial cardiac baroreceptor reflex, but the mechanisms and sites of action are unknown. This study tested the hypothesis that DIO impairs central aortic baroreceptor pathways. Normal chow control (CON) and high-fat-chow obesity-resistant (OR) and obesity-prone (OP) rats were anesthetized (inactin, 120 mg/kg) and underwent sinoaortic denervation. The central end of the aortic depressor nerve (ADN) was electrically stimulated to generate frequency-dependent baroreflex curves (5-100 Hz) during selective activation of myelinated (A-fiber) or combined (A-and C-fiber) ADN baroreceptors. A mild stimulus (1 V) that activates only A-fiber ADN baroreceptors induced robust, frequency-dependent depressor and bradycardic responses in CON and OR rats, but these responses were completely abolished in OP rats. Maximal activation of A fibers (3 V) elicited frequency-dependent reflexes in all groups, but a dramatic deficit was still present in OP rats. Activation of all ADN baroreceptors (20 V) evoked even larger reflex responses. Depressor responses were nearly identical among groups, but OP rats still exhibited attenuated bradycardia. In separate groups of rats, the reduced heart rate (HR) response to maximal activation of ADN A fibers (3 V) persisted in OP rats following pharmacological blockade of ␤1-adrenergic or muscarinic receptors, suggesting deficits in both parasympathetic nervous system (PNS) and sympathetic nervous system (SNS) reflex pathways. However, the bradycardic responses to direct efferent vagal stimulation were similar among groups. Taken together, our data suggest that DIO severely impairs the central processing of myelinated aortic baroreceptor control of HR, including both PNS and SNS components. obesity; autonomic nervous system; arterial baroreflex OBESITY IS ASSOCIATED WITH multisystem morbidity, including endocrine, immune, and autonomic manifestations (3,8,28), such as impairment of the baroreceptor reflex pathways. The depression of baroreceptor reflex sensitivity during weight gain in humans (4, 21) is replicated in animal models of obesity (9,24,25,39,40). Furthermore, the restoration of baroreflex function with weight loss suggests a dynamic interrelationship between diet, metabolic status, and cardiovascular autonomic control (4,21,41,42). Obesity not only increases sympathetic outflow (SNS) to muscle (1, 21) and kidneys (45), but it also decreases cardiac parasympathetic (PNS) drive (6, 36). Because a depressed cardiac PNS baroreflex is an important predictor of cardiac morbidity and mortality (29), independent of blood pressure changes, the mechanisms responsible for baroreflex modification during obesity are critical to understand.Changes in arterial pressure are transmitted via the arterial baroreceptors to the...

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“…10 Blunted BRS in obese animals and humans also represents a negative prognostic factor in cardiovascular diseases and may lead to long-term cardiovascular mortality. 7,34 The development of blunted BRS in obesity is insidious and may often be overlooked because patients are typically free of complaints. Our current finding that the blunted BRS in obese Zucker rats is, at least in part, attributed to altered nitroxidergic or NMDA receptor-mediated modulation provides a possible explanation for the development of blunted BRS in obesity.…”

Section: Significancementioning

confidence: 99%

“…1 The impulses triggered by arterial baroreceptors are propagated through the glossopharyngeal and vagus nerves to the nucleus tractus solitarii of the medulla, resulting in inhibition of the sympathetic system and activation of the parasympathetic system. [3][4] Baroreflex sensitivity (BRS) has often been reported to be impaired or reduced in normotensive obese subjects, 5 hypertensive patients with central obesity, 6 obese women, 7 young and older obese men, 8 and obese patients with metabolic syndrome. 9 The underlying mechanism of baroreflex attenuation in obesity is not yet well known; however, there is increasing evidence that it is at least partly related to autonomic nervous system dysfunction and particularly to the sympathetic overactivity that accompanies obesity.…”

Section: Introductionmentioning

confidence: 99%

“…[20][21] It is important to note that reduced baroreflex sensitivity, which is common in obesity, may contribute to the increased risk of cardiovascular disease and represents a negative prognostic factor in cardiovascular diseases. 7,9 Neurotransmission or neuromodulation has a crucial role in the processing of neural signals for coordinating arterial baroreflex control. 22 The neuromodulatory effect of nitroxidergic and glutamatergic transmission has been reported to be involved in baroreflex regulation.…”

Section: Introductionmentioning

confidence: 99%

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Altered nitroxidergic and NMDA receptor-mediated modulation of baroreflex-mediated heart rate in obese Zucker rats

et al. 2010

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Arterial baroreflex, an important physiological regulatory system for buffering systemic blood pressure, is impaired in obesity. This study investigated whether the blunted baroreflex function in obesity is attributed to the altered nitroxidergic or N-methyl-Daspartate (NMDA) mechanism. Baroreflex bradycardia responses, blood pressure and heart rate in 30 lean and 30 obese anesthetized Zucker rats (8-12 weeks of age) were assessed after injecting phenylephrine with intravenous preadministration of saline (control), dextromethorphan (DXM, NMDA receptor antagonist, 10 mg kg À1 ) or N(G)-nitro-L-arginine methyl ester (L-NAME, nitric oxide synthase inhibitor, 100 mg kg À1 ). Compared with lean rats (À2.00 ± 0.29 b.p.m. mm Hg À1 ), the baroreflex sensitivity (BRS) in obese rats (-0.43±0.05 b.p.m. mm Hg À1 ) was significantly blunted. The BRS was significantly suppressed by DXM in lean rats but not in obese rats. After administration of L-NAME, BRS was significantly suppressed in lean Zucker rats but not in obese Zucker rats. The normal BRS was significantly suppressed in lean rats after administration of both DXM and L-NAME, and the blunted BRS in obesity was significantly blocked to nearly no BRS after administration of both DXM and L-NAME. This study suggests that BRS is blunted in obese rats and that blunted baroreflex is, at least in part, attributed to altered nitroxidergic or NMDA receptor-mediated modulation.

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Baroreflex Sensitivity in Obesity: Relationship With Cardiac Autonomic Nervous System Activity

Cited by 127 publications

References 47 publications

Body fat, especially visceral fat, is associated with electrocardiographic measures of sympathetic activation

Body fat, especially visceral fat, is associated with electrocardiographic measures of sympathetic activation

Diet-induced obesity severely impairs myelinated aortic baroreceptor reflex responses

Altered nitroxidergic and NMDA receptor-mediated modulation of baroreflex-mediated heart rate in obese Zucker rats

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