Evidence for Pressure‐Independent Sympathetic Modulation of Central Pulse Wave Velocity

Nardone, Massimo; Incognito, Anthony V.; Millar, Philip J.

doi:10.1161/jaha.117.007971

Cited by 47 publications

(32 citation statements)

References 57 publications

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“…26 The limitation of changes in MAP when modulating MSNA has been overcome in some studies by examining carotid-femoral PWV in response to application of mild lower body negative pressure (LBNP), which elicits reflex increases in MSNA and vasoconstriction without increases in MAP. [30][31][32] However, these studies have been performed primarily in young adults, and therefore it remains unclear whether carotid-femoral PWV is modulated by acute changes in MSNA independent of MAP in MA/O adults.…”

Section: Introductionmentioning

confidence: 99%

Elevated Muscle Sympathetic Nerve Activity Contributes to Central Artery Stiffness in Young and Middle-Age/Older Adults

Holwerda¹,

Luehrs²,

DuBose

et al. 2019

Hypertension

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Muscle sympathetic neural activity (MSNA) influences the mechanical properties (i.e., vascular smooth muscle tone and stiffness) of peripheral arteries, but it remains controversial whether MSNA contributes to stiffness of central arteries such as the aorta and carotids. We examined whether elevated MSNA (age-related) would be independently associated with greater stiffness of central [carotid-femoral pulse wave velocity (PWV)] and peripheral (carotid-brachial PWV) arteries, in addition to lower carotid compliance coefficient (CC), in healthy men and women (n=88, age:19-73 years, 52%men). Also, we examined whether acute elevations in MSNA without increases in mean arterial pressure (MAP) using graded levels of lower body negative pressure (LBNP) would augment central and peripheral artery stiffness in young (YG, n=15, 60%men) and middle-age/older adults (MA/O, n=14, 43%men). Resting MSNA burst frequency (bursts•min −1) was significantly correlated with carotid-femoral PWV (R=0.44, P<0.001), carotid-brachial PWV (R=0.32, P=0.003), and carotid CC (R=0.28, P=0.01) after controlling for sex, MAP, heart rate, and waist-to-hip ratio (central obesity), but these correlations were abolished after further controlling for age (all P>0.05). In YG and MA/O adults, MSNA was elevated during LBNP (P<0.001) and produced significant increases in carotid-femoral PWV (YG:Δ+1.3±0.3 vs. MA/ O:Δ+1.0±0.3 m•s −1 , P=0.53) and carotid-brachial PWV (YG: Δ+0.7±0.3 vs. MA/O: Δ+0.7±0.5 m•s −1 , P=0.92), whereas carotid CC during LBNP was significantly reduced in YG but not MA/O (YG:Δ-0.04 ±0.01 vs. MA/O:Δ0.001±0.008 mm 2 •mmHg −1 , P<0.01). Collectively, these data demonstrate the influence of MSNA on central artery stiffness and its potential contribution to age-related increases in stiffness of both peripheral and central arteries.

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Section: Introductionmentioning

confidence: 99%

Elevated Muscle Sympathetic Nerve Activity Contributes to Central Artery Stiffness in Young and Middle-Age/Older Adults

Holwerda¹,

Luehrs²,

DuBose

et al. 2019

Hypertension

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“…Considering that endothelial dysfunction, one of the key mechanisms for increased arterial stiffness, is largely precipitated by systemic inflammation, and that CST has speculated immunomodulatory roles, it is possible that CST could have a role in the interconnection of IBD and cardiovascular diseases [3]. From another aspect, sympathetic nervous system (SNS) activity might be an important contributor to pathologic arterial remodeling and this might translate to increased arterial stiffness parameters as postulated in previous clinical studies [54][55][56]. Importantly, sympathetic overactivity is present in patients with ulcerative colitis [57,58].…”

Section: Discussionmentioning

confidence: 94%

Serum Catestatin Levels and Arterial Stiffness Parameters Are Increased in Patients with Inflammatory Bowel Disease

Živković

Matetić

Hadjina

et al. 2020

JCM

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Catestatin (CST) is an important peptide in the pathophysiology of chronic inflammatory disorders. However, clinical studies on inflammatory bowel disease (IBD) patients are lacking. Our goal was to investigate CST concentrations in IBD patients compared to healthy subjects. Additionally, we aimed to determine arterial stiffness parameters in relation to CST. This cross-sectional study compared 80 IBD patients (45 Crohn’s disease (CD) and 35 ulcerative colitis (UC) patients) with 75 control subjects. Serum CST levels were significantly higher in the IBD group compared to control subjects (11.29 ± 9.14 vs. 7.13 ± 6.08 ng/mL, p = 0.001) and in the UC group compared to CD patients (13.50 ± 9.58 vs. 9.03 ± 6.92 ng/mL, p = 0.021), irrespective of age and BMI. IBD patients exhibited significantly higher values of heart rate adjusted central augmentation index (cAIx-75) (14.88 ± 10.59 vs. 6.87 ± 9.50 %, p < 0.001) and pulse wave velocity (PWV) (8.06 ± 3.23 vs. 6.42 ± 1.47 m/s, p < 0.001) compared to control group. Furthermore, PWV was the only significant independent correlate of CST (B = 1.20, t = 4.15, p < 0.001), while CST, PWV, cAIx-75, high-sensitivity C-reactive protein and BMI were significant predictors of positive IBD status (1.089 (1.022–1.161), 1.515 (1.166–1.968), 1.060 (1.024–1.097), 1.458 (1.116–1.906), 0.793 (0.683–0.920), respectively). Serum CST levels were significantly higher in IBD patients compared to controls and an independent positive correlation of CST with PWV existed. Therefore, it is possible that CST could have a role in the complex pathophysiology of IBD and its cardiovascular complications.

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“…61,62 Moreover, high sympathetic overactivity and alterations in NO synthesis attributable to accumulation of the endogenous NO synthase inhibitor ADMA have been identified as potential causal mechanisms for the high CV mortality rates among patients with ESRD. 33 Finally, the sympathetic hyperactivity could be also considered a maladaptive mechanism to respond to the reduced stimulation of the baroreceptors, and an important part of a vicious circle: peripheral sympathetic hyperactivity leading to increased arterial stiffness, 63 leading to baroreflex dysfunction, 60 leading to peripheral sympathetic hyperactivity.…”

Section: Arterial Stiffening and Baroreflex Dysfunctionmentioning

confidence: 99%

Arterial Stiffness in the Heart Disease of CKD

Zanoli

Lentini

Briet

et al. 2019

JASN

155

130

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CKD frequently leads to chronic cardiac dysfunction. This complex relationship has been termed as cardiorenal syndrome type 4 or cardio-renal link. Despite numerous studies and reviews focused on the pathophysiology and therapy of this syndrome, the role of arterial stiffness has been frequently overlooked. In this regard, several pathogenic factors, including uremic toxins (i.e., uric acid, phosphates, endothelin-1, advanced glycation end-products, and asymmetric dimethylarginine), can be involved. Their effect on the arterial wall, direct or mediated by chronic inflammation and oxidative stress, results in arterial stiffening and decreased vascular compliance. The increase in aortic stiffness results in increased cardiac workload and reduced coronary artery perfusion pressure that, in turn, may lead to microvascular cardiac ischemia. Conversely, reduced arterial stiffness has been associated with increased survival. Several approaches can be considered to reduce vascular stiffness and improve vascular function in patients with CKD. This review primarily discusses current understanding of the mechanisms concerning uremic toxins, arterial stiffening, and impaired cardiac function, and the therapeutic options to reduce arterial stiffness in patients with CKD.

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Evidence for Pressure‐Independent Sympathetic Modulation of Central Pulse Wave Velocity

Cited by 47 publications

References 57 publications

Elevated Muscle Sympathetic Nerve Activity Contributes to Central Artery Stiffness in Young and Middle-Age/Older Adults

Elevated Muscle Sympathetic Nerve Activity Contributes to Central Artery Stiffness in Young and Middle-Age/Older Adults

Serum Catestatin Levels and Arterial Stiffness Parameters Are Increased in Patients with Inflammatory Bowel Disease

Arterial Stiffness in the Heart Disease of CKD

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