Regulation of Arterial Stiffness: Cellular, Molecular and Neurogenic Mechanisms☆

Avolio, Alberto; Butlin, Mark; Liu, Yingli; Viegas, Kayla; Avadhanam, Bhargava; Lindesay, George

doi:10.1016/j.artres.2011.10.002

Cited by 19 publications

(7 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Endothelial cells decrease the usual production of nitric oxide (NO) and increase endothelin (E1), favoring arterial stiffness. In turn, arterial stiffness subsequently alters the endothelium, thus generating a vicious circle ( 27 , 28 ).…”

Section: One Way: From Chronic Kidney Disease To Vascular Injurymentioning

confidence: 99%

Chronic Kidney Disease and Arterial Stiffness: A Two-Way Path

et al. 2021

View full text Add to dashboard Cite

The kidney-heart relationship has raised interest for the medical population since its vast and complex interaction significantly impacts health. Chronic kidney disease (CKD) generates vascular structure and function changes, with significant hemodynamic effects. The early arterial stiffening in CKD patients is a consequence of the interaction between oxidative stress and chronic vascular inflammation, leading to an accelerated deterioration of left ventricular function and alteration in tissue perfusion. CKD amplifies the inflammatory cascade's activation and is responsible for altering the endothelium function, increasing the vascular tone, wall thickening, and favors calcium deposits in the arterial wall. Simultaneously, the autonomic imbalance, and alteration in other hormonal systems, also favor the overactivation of inflammatory and fibrotic mediators. Thus, hormonal disarrangement also contributes to structural and functional lesions throughout the arterial wall. On the other hand, a rise in arterial stiffening and volume overload generates high left ventricular afterload. It increases the left ventricular burden with consequent myocardial remodeling, development of left ventricular hypertrophy and, in turn, heart failure. It is noteworthy that reduction in glomerular mass of renal diseases generates a compensatory glomerular filtration overdriven associated with large-arteries stiffness and high cardiovascular events. Furthermore, we consider that the consequent alterations of the arterial system's mechanical properties are crucial for altering tissue perfusion, mainly in low resistance. Thus, increasing the knowledge of these processes may help the reader to integrate them from a pathophysiological perspective, providing a comprehensive idea of this two-way path between arterial stiffness and renal dysfunction and their impact at the cardiovascular level.

show abstract

Section: One Way: From Chronic Kidney Disease To Vascular Injurymentioning

confidence: 99%

Chronic Kidney Disease and Arterial Stiffness: A Two-Way Path

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Therefore, the endothelium is the key regulator of blood pressure and vascular tone. Deterioration of endothelial function and smooth muscle tone lead to the stiffening of elastic and muscular arteries [25]. Vasoconstrictors, such as noradrenaline, endothelin-1 (ET-1) or angiotensin II (Ang II), increase artery stiffness [26,27], whereas vasodilators such as glyceryl trinitrate elicit opposite effects [27][28][29][30].…”

Section: Improvement Of Endothelial Functionmentioning

confidence: 99%

“…Arterial stiffening represents the sum of the passive stiffness, which is mainly contributed to by elastic and collagen fibres, and the active stiffness generated by the smooth muscle tone [79]. Changes in endothelial function and smooth muscle tone can influence the stiffness of the elastic and muscular arteries [25]. Although the stiffening of vasculature is a universal change associated with aging, it is also part of the phenotype in diseases such as hypertension and diabetes where complex cellular mechanisms conspire to accentuate arterial remodelling.…”

Section: Prevention Of Arterial Stiffeningmentioning

confidence: 99%

Resveratrol and the Interaction between Gut Microbiota and Arterial Remodelling

Man

Xia

2020

Nutrients

View full text Add to dashboard Cite

Arterial remodelling refers to the alteration in the structure of blood vessel that contributes to the progression of hypertension and other cardiovascular complications. Arterial remodelling is orchestrated by the crosstalk between the endothelium and vascular smooth muscle cells (VSMC). Vascular inflammation participates in arterial remodelling. Resveratrol is a natural polyphenol that possesses anti-oxidant and anti-inflammatory properties and has beneficial effects in both the endothelium and VSMC. Resveratrol has been studied for the protective effects in arterial remodelling and gut microbiota, respectively. Gut microbiota plays a critical role in the immune system and inflammatory processes. Gut microbiota may also regulate vascular remodelling in cardiovascular complications via affecting endothelium function and VSMC proliferation. Currently, there is new evidence showing that gut microbiota regulate the proliferation of VSMC and the formation of neointimal hyperplasia in response to injury. The change in population of the gut microbiota, as well as their metabolites (e.g., short-chain fatty acids) could critically contribute to VSMC proliferation, cell cycle progression, and migration. Recent studies have provided strong evidence that correlate the effects of resveratrol in arterial remodelling and gut microbiota. This review aims to summarize recent findings on the resveratrol effects on cardiovascular complications focusing on arterial remodelling and discuss the possible interactions of resveratrol and the gut microbiota that modulate arterial remodelling.

show abstract

“…«Пассивные» механизмы сосудистой жесткости обусловлены состоянием эластических и коллагеновых волокон в стенке артерии, сердечным ритмом (большая ЧСС связана с повышенной артериальной жесткостью) [47] и, по-видимому, генетическим полиморфизмом [34]. «Активные» механизмы, модулирующие артериальную жесткость, включают эндотелиальную функцию [48], низкоинтенсивное воспаление и окислительный стресс в сосудистой стенке, тонус симпатической нервной системы [49]. Степень влияния пассивного и активного (функционального) компонентов регуляции жесткости стенки зависит от типа артерии: бóльшее влияние функционального компонента наблюдается в артериях мышечного типа (сонная и плечевая артерии) по сравнению с артериями эластического типа (аорта) [34].…”

Section: оригинальные статьи § обсуждениеunclassified

Daily variability of arterial stiffness of patients with arterial hypertension depending on the category of cardiovascular risk

Tarlovskaya

Merezhanova

2018

Kardiologiia

View full text Add to dashboard Cite

Purpose. The study of the daily variability of arterial stiffness indicators, depending on the category of cardiovascular risk. Materials and methods. The study consistently included patients with essential hypertension who were admitted to the cardiology department of the Volga district medical center from November 1, 2015 to October 1, 2017. The study involved 134 patients with an average age of 52±1 years. Depending on the category of total cardiovascular risk, the patients were divided into 3 groups from I (lowest risk) to III (highest risk). The analysis was carried out on ABPM for 12–14 days (BPLab system of “Peter Telegin” firm). Determined: glomerular filtration rate (GFR), the thickness of the intima-media of the common carotid arteries, analysis of the lipid spectrum. For statistical analysis of clinical and instrumental data, a T-criterion for independent samples was used and an ANOVA analysis was performed. A correlation analysis was performed. Results. Patients of group III had the highest level of av. SBP (рI–III=0.010; pII–III=0.020) and mean pulse BP (PBP) (рI–III=0.002; pII–III=0.002), also more unfavorable the indicators cALALx (pI–II=0.025; рI–III=0.004), varAlx (рI–III=0.004) and av. ASI (рI–III=0.034). When comparing the data of patients of groups II and III, adjusted for gender and age, it was found that statistically significant differences between the groups of varPAD (pII–III=0.008), AASI (рI–III=0.043), varAlx (pII–III=0.049), as well as a pronounced tendency for varASI (pII–III=0.050). Markers of target organ damage (TIM, LVML, GFR) were more pronounced in the high-risk group. As the risk group increased, the level of HDL decreased (рI–III=0.002; pII–IIII=0.0001), the level of TG increased (рI–III=0.007; pII–III=0.009) and the CA (рI–III=0.015). The total cholesterol level was lower in patients of group III compared to group II (pII–III=0.004). Statistically signifi nt relationships of arterial wall stiffness indicators with age were found: crAlx (0.467, p<0.001), varAlx (0.272, p<0.01), cpASI (0.227, p<0.01), varASI (0.407, p<0.001). In addition, women showed significant correlations of medium and high strength between age and mean values of mean SPD (r = 0.490, p<0.05), varPAD (r=0.540, p<0.05), avAS (r=0.460, p<0.05) and varASI (r=0.620, p<0.05). VarASI and WedSASI were most closely associated with the level of SRSAD and SRPAD. Only cASI was associated with GFR, and only varASI was associated with the parameters of the lipid spectrum (HSLPVP, TG, KA and LVMI. Conclusion. The most statistically significant dynamics was observed when evaluating varASI, which varied in the sequence I gr. <II gr. < III gr. Corrected by sex and age, the analysis showed a greater variability in arterial stiffness in high-risk patients.

show abstract

Regulation of Arterial Stiffness: Cellular, Molecular and Neurogenic Mechanisms☆

Cited by 19 publications

References 52 publications

Chronic Kidney Disease and Arterial Stiffness: A Two-Way Path

Chronic Kidney Disease and Arterial Stiffness: A Two-Way Path

Resveratrol and the Interaction between Gut Microbiota and Arterial Remodelling

Daily variability of arterial stiffness of patients with arterial hypertension depending on the category of cardiovascular risk

Contact Info

Product

Resources

About