Sympathetic activation markedly reduces endothelium-dependent, flow-mediated vasodilation

Hijmering, Michel L.; Stroes, Erik S.G.; Olijhoek, Jobien K.; Hutten, Barbara A.; Blankestijn, Peter J.; Rabelink, Ton J.

doi:10.1016/s0735-1097(01)01786-7

Cited by 313 publications

(263 citation statements)

References 36 publications

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“…EAT related to endothelial dysfunction assessed by flow-mediated dilatation of the brachial artery, in patients with metabolic syndrome (MS) (Aydin et al 2010). Furthermore, increased sympathetic activation and decreased vagal activity may markedly suppress endothelial function (Hijmering et al 2002;Huang et al 2004). Şengül and Duman (2011) reported that EAT was significantly associated with blunted heart rate recovery in patients with MS. A recent study revealed a linear and negative correlation between aortic diameters and endothelium dependent vasodilation (Medina et al 2010).…”

Section: Discussionmentioning

confidence: 99%

Increased Epicardial Adipose Tissue Thickness Is Correlated with Ascending Aortic Diameter

Çanğa

Kocaman

Çetin

et al. 2012

Tohoku J. Exp. Med.

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Epicardial adipose tissue (EAT), localized beneath the visceral pericardium, is a metabolically active endocrine and paracrine organ with possible interactions within the heart. Recent studies identified possible roles of uric acid (UA)-induced oxidative stress and increased inflammatory status in the pathogenesis of ascending aortic dilatation. The aim of this study was to investigate whether EAT is an independent factor for ascending aortic dilatation. The patients were evaluated by a complete transthoracic echocardiographic examination including measurements of EAT and aortic dimensions. Serum levels of UA and C-reactive protein and EAT thicknesses were compared in 38 patients with dilated ascending aorta (DAA) (the diameter ≥ 37 mm) vs. 107 subjects with normal aortic diameter (AD) of < 37 mm. EAT thickness was significantly higher in DAA group compared to normal AD group (8.3 ± 2.7 vs. 5.4 ± 2.2 mm, p < 0.001) as well as age (53 ± 10 vs. 48 ± 9 years, p = 0.004), the presence of hypertension (54% vs. 30%, p = 0.009) and UA levels (6.0 ± 1.4 vs. 5.2 ± 1.1 mg/dL, p < 0.001). There was a strong correlation between EAT thickness and ascending aortic diameter (r = 0.521, p < 0.001). In multiple logistic regression analysis, EAT thickness (OR: 1.429, p = 0.006), body mass index (OR: 1.169, p = 0.014) and UA levels (OR: 1.727, p = 0.023) were independently correlated to ascending aortic dilatation. We therefore propose that increased EAT thickness is an independent predictor of ascending aortic dilation.

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Section: Discussionmentioning

confidence: 99%

Increased Epicardial Adipose Tissue Thickness Is Correlated with Ascending Aortic Diameter

Çanğa

Kocaman

Çetin

et al. 2012

Tohoku J. Exp. Med.

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“…Flow-mediated dilation is commonly used for this purpose, but measures mostly the role of eNO in conduit arteries and may be influenced by sympathetic tone. 12 Forearm blood flow responses to intrabrachial infusion of endothelial-dependent vasodilators are also used for this purpose. This approach provides important information about endothelial function, 25 and forearm responses correlate with those of other vascular beds, most notably the coronary circulation.…”

Section: Discussionmentioning

confidence: 99%

“…11 This response, however, seems to be influenced by sympathetic activity. 12,13 Therefore, it is difficult to estimate how important eNO is to overall blood pressure regulation from the use of these conventional methods.…”

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confidence: 99%

Contribution of Endothelial Nitric Oxide to Blood Pressure in Humans

Gamboa¹,

Shibao²,

Diedrich³

et al. 2007

Hypertension

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Abstract-Impaired endothelial-derived NO (eNO) is invoked in the development of many pathological conditions. Systemic inhibition of NO synthesis, used to assess the importance of NO to blood pressure (BP) regulation, increases BP by Ϸ15 mm Hg. This approach underestimates the importance of eNO, because BP is restrained by baroreflex mechanisms and does not account for a role of neurally derived NO. To overcome these limitations, we induced complete autonomic blockade with trimethaphan in 17 normotensive healthy control subjects to eliminate baroreflex mechanisms and contribution of neurally derived NO. Under these conditions, the increase in BP reflects mostly blockade of tonic eNO. N G -Monomethyl-L-arginine (250 g/kg per minute IV) increased mean BP by 6Ϯ3.7 mm Hg (from 77 to 82 mm Hg) in intact subjects and by 21Ϯ8.4 mm Hg (from 75 to 96 mm Hg) during autonomic blockade. We did not find a significant contribution of neurally derived NO to BP regulation after accounting for baroreflex buffering. To further validate this approach, we compared the effect of NOS inhibition during autonomic blockade in 10 normotensive individuals with that of 6 normotensive smokers known to have endothelial dysfunction but who were otherwise normal. As expected, normotensive smokers showed a significantly lower increase in systolic BP during selective eNO blockade (11Ϯ4.

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“…In particular, several lines of evidence suggest that NO tonically suppresses sympathetic tone (22,31), and impaired NO function could contribute to the sympathetic activation observed in hypertension. Conversely, sympathetic activation can impair NO function (9). It is possible, therefore, that these interactions between NO and the sympathetic nervous system, rather than a primary impairment of NO-mediated dilation, contribute to hypertension.…”

mentioning

confidence: 99%

Sympathetic activation and nitric oxide function in early hypertension

Gamboa

Okamoto²,

Diedrich³

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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The purpose of this study was to determine if tonic restrain of blood pressure by nitric oxide (NO) is impaired early in the development of hypertension. Impaired NO function is thought to contribute to hypertension, but it is not clear if this is explained by direct effects of NO on vascular tone or indirect modulation of sympathetic activity. We determined the blood pressure effect of NO synthase inhibition with N -monomethyl-L-arginine (L-NMMA) during autonomic blockade with trimethaphan to eliminate baroreflex buffering and NO modulation of autonomic tone. In this setting, impaired NO modulation of vascular tone would be reflected as a blunted pressor response to L-NMMA. We enrolled a total of 66 subjects (39 Ϯ 1.3 yr old, 30 females), 20 normotensives, 20 prehypertensives (blood pressure between 120/80 and 140/90 mmHg), 17 hypertensives, and 9 smokers (included as "positive" controls of impaired NO function). Trimethaphan normalized blood pressure in hypertensives, suggesting increased sympathetic tone contributing to hypertension. In contrast, L-NMMA produced similar increases in systolic blood pressure in normal, prehypertensive, and hypertensive subjects (31 Ϯ 2, 32 Ϯ 2, and 30 Ϯ 3 mmHg, respectively), whereas the response of smokers was blunted (16 Ϯ 5 mmHg, P ϭ 0.012). Our results suggest that sympathetic activity plays a role in hypertension. NO tonically restrains blood pressure by ϳ30 mmHg, but we found no evidence of impaired modulation by NO of vascular tone contributing to the early development of hypertension. If NO deficiency contributes to hypertension, it is likely to be through its modulation of the autonomic nervous system, which was excluded in this study.hypertension; nitric oxide; nervous system; autonomic; nervous system; sympathetic; nitric oxide synthase NITRIC OXIDE (NO) is arguably the most important metabolic modulator of blood pressure (BP); our previous studies suggest that NO tonically restrains BP by at least 30 mmHg in healthy young adults (6). Not surprisingly, there has been great interest in determining if impaired NO function plays a role in hypertension. Reduced NO production (5) or bioavailability (1), or impaired NO-mediated vasodilation (17), have been implicated in the development or maintenance of hypertension (2). There is, indeed, significant evidence that NO function is impaired in hypertension, but the precise mechanism underlying this problem is less clear. There are at least two mechanisms by which NO can lower BP. NO, derived from endothelial cells or from nitrergic nerves, tonically produces vasodilatation. NO also interacts with the sympathetic nervous system at multiple levels and, through this interaction, can modulate BP. In particular, several lines of evidence suggest that NO tonically suppresses sympathetic tone (22,31), and impaired NO function could contribute to the sympathetic activation observed in hypertension. Conversely, sympathetic activation can impair NO function (9). It is possible, therefore, that these interactions between NO and the symp...

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Sympathetic activation markedly reduces endothelium-dependent, flow-mediated vasodilation

Abstract: Sympathetic stimulation, at a clinically relevant range, significantly impairs the FMD response by an alpha-adrenergic mechanism.

Cited by 313 publications

References 36 publications

Increased Epicardial Adipose Tissue Thickness Is Correlated with Ascending Aortic Diameter

Increased Epicardial Adipose Tissue Thickness Is Correlated with Ascending Aortic Diameter

Contribution of Endothelial Nitric Oxide to Blood Pressure in Humans

Sympathetic activation and nitric oxide function in early hypertension

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