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Daming capsule restores endothelial dysfunction induced by high-fat diet
Rong Zhang, Huifang Niu, Ning Wang, Lihua Sun, Yi Xu, Ruibo Zhao, Xiang Ban, Yao Yu, Baofeng Yang, Jing Ai
BMC Complementary and Alternative Medicine , 2012, DOI: 10.1186/1472-6882-12-21
Abstract: Rats were divided into four groups: control, HF diet, HF mixed DMC diet, HF mixed atorvastatin (ATV) diet. After 30 days, the thoracic cavity was exposed to remove the thoracic aorta for (i) histological examination; (ii) measurement of endothelial nitric oxide synthase (eNOS) by western blot; and (iii) tension study of thoracic aortic ring.HF diet induced significant attenuation in the contraction and relaxation of rat aortic rings. Treatment with DMC significantly improved the relaxation of the aortic rings as compared with those from HF rats (P < 0.05), which was abolished by a nonspecific NOS inhibitor L-NAME. Moreover DMC significantly restored the decrease in eNOS expression induced by HF diet. Similar results were found in histopathologic changes. DMC failed to restore the loss of vasocontraction of aorta explained by an impairment of ATP-sensitive K+ channels (KATP) on the structure and/or function. DMC exerted the same protective effect as ATV, a positive control drug, on vascular injury produced by HF diet.DMC partially protects the aorta from HF-induced endothelial dysfunction via upregulation of the expression of eNOS.Hyperlipidemia is an important independent risk factor for cardiovascular diseases. Hyperlipidemia is accompanied by vascular disease such as: atherosclerosis, angiostenosis and blocking, which may induce hypertension, cerebral apoplexy, myocardial infarction, and even sudden cardiac death. Accumulating evidence indicates that a high-fat diet induces both systemic and tissue oxidative stress and the development of early vascular lesions [1]. Impaired endothelial function, an early hallmark of atherogenesis, was observed in rats and healthy volunteers fed high-saturated fat and high-sucrose meals [2,3]. Moreover, nitric oxide (NO) produced by endothelium was inhibited by high-fat diet [4]. Hyperlipidemia and oxidation of low density lipoprotein (LDL) induce vascular smooth muscle cell growth [5] and hyperlipidemia may alter the vascular resp
Effect of Aging and Dietary Salt and Potassium Intake on Endothelial PTEN (Phosphatase and Tensin Homolog on Chromosome 10) Function  [PDF]
Wei-Zhong Ying,Kristal J. Aaron,Paul W. Sanders
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0048715
Abstract: Aging promotes endothelial dysfunction, defined as a reduction in bioavailable nitric oxide (NO) produced by the endothelial isoform of nitric oxide synthase (NOS3). This enzyme is critically regulated by phosphorylation by protein kinase B (Akt), which in turn is regulated by the lipid phosphatase, PTEN. The present series of studies demonstrated a reduction in bioavailable NO as the age of rats increased from 1 to 12 months. At 12 months of age, rats no longer demonstrated increases in phosphorylated NOS3 in response to high dietary salt intake. Endothelial cell levels of PTEN increased with age and became refractory to change with increased salt intake. In contrast to the reduction in NO production, endothelial cell production of transforming growth factor-? (TGF-?) relative to NO increased progressively with age. In macrovascular endothelial cells, PTEN was regulated in a dose-dependent fashion by TGF-?, which was further regulated by extracellular [KCl]. When combined with prior studies, the present series of experiments suggested an integral role for PTEN in endothelial cell pathobiology of aging and an important mitigating function of TGF-? in endothelial PTEN regulation. The findings further supported a role for diet in affecting vascular function through the production of TGF-? and NO.
Consumption of High-Polyphenol Dark Chocolate Improves Endothelial Function in Individuals with Stage 1 Hypertension and Excess Body Weight  [PDF]
Lívia de Paula Nogueira,Marcela Paranhos Knibel,Márcia Regina Simas Gon?alves Torres,José Firmino Nogueira Neto,Antonio Felipe Sanjuliani
International Journal of Hypertension , 2012, DOI: 10.1155/2012/147321
Abstract: Background. Hypertension and excess body weight are important risk factors for endothelial dysfunction. Recent evidence suggests that high-polyphenol dark chocolate improves endothelial function and lowers blood pressure. This study aimed to evaluate the association of chocolate 70% cocoa intake with metabolic profile, oxidative stress, inflammation, blood pressure, and endothelial function in stage 1 hypertensives with excess body weight. Methods. Intervention clinical trial includes 22 stage 1 hypertensives without previous antihypertensive treatment, aged 18 to 60 years and presents a body mass index between 25.0 and 34.9?kg/m2. All participants were instructed to consume 50?g of chocolate 70% cocoa/day (2135?mg polyphenols) for 4 weeks. Endothelial function was evaluated by peripheral artery tonometry using Endo-PAT 2000 (Itamar Medical). Results. Twenty participants (10 men) completed the study. Comparison of pre-post intervention revealed that (1) there were no significant changes in anthropometric parameters, percentage body fat, glucose metabolism, lipid profile, biomarkers of inflammation, adhesion molecules, oxidized LDL, and blood pressure; (2) the assessment of endothelial function through the reactive hyperemia index showed a significant increase: 1.94 ± 0.18 to 2.22 ± 0.08, . Conclusion.In individuals with stage 1 hypertension and excess body weight, high-polyphenol dark chocolate improves endothelial function. 1. Introduction The endothelium has emerged as a key regulator of vascular homeostasis, acting as an active signal transducer for metabolic, hemodynamic, and inflammatory factors that modify the function and morphology of the vessel wall. Alterations in endothelial-cell function can precede the development of atherosclerotic changes and the progression of cardiovascular diseases [1]. Hypertension and excess body weight (body mass index (BMI) ≥25?kg/m2) are conditions with high prevalence, being important risk factors for endothelial dysfunction [2–5]. According to World Health Organization (2009) [3] high blood pressure is responsible for 13% of deaths globally and overweight and obesity are responsible for 5%. Hypertension and obesity are frequently associated, and the causal association between obesity and elevated blood pressure has since long been demonstrated [6]. Lifestyle interventions, including diet, may affect endothelial function: high-fat diets impair endothelial function, and diets such as the Mediterranean diet are associated with improved endothelial function [7]. Recently, cocoa and cocoa-derived products such as
Endothelial function within adolescents with cardiovascular risk  [cached]
Vladimir Strogiy,Tatiana Woitovich,Marina Borisionok,Natalia Zimnickaya
Medical and Health Science Journal , 2010,
Abstract: Cardiovascular diseases represent the major medical and social problem. The main idea of this article was to estimate the earliest markers of vascular system injury. Endothelial function among teenagers with arterial hypertension and dyslipidemia were studied by ultrasound method, and von Willebrand factor was determined in blood. Endothelial function was changed in 46.9% of persons. Various characters of disturbances of endothelial functions were revealed.
Insomnia and Endothelial Function – The HUNT 3 Fitness Study  [PDF]
Linn B. Strand, Lars E. Laugsand, Eli-Anne Skaug, ?yvind Ellingsen, Erik Madssen, Ulrik Wisl?ff, Lars Vatten, Imre Janszky
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0050933
Abstract: Background Insomnia is associated with increased risk of coronary heart disease (CHD), but the underlying mechanisms are not understood. To our knowledge, no previous studies have examined insomnia in relation to endothelial function, an indicator of preclinical atherosclerosis. Our aim was to assess the association of insomnia with endothelial function in a large population based study of healthy individuals. Methods A total of 4 739 participants free from known cardiovascular or pulmonary diseases, cancer, and sarcoidosis, and who were not using antihypertensive medication were included in the study. They reported how often they had experienced difficulties falling asleep at night, repeated awakenings during the night, early awakenings without being able to go back to sleep, and daytime sleepiness. Endothelial function was measured by flow mediated dilation (FMD) derived from the brachial artery. Results We found no consistent association between the insomnia symptoms and endothelial function in multiadjusted models, but individual insomnia symptoms may be related to endothelial function. Among women who reported early awakenings, endothelial function may be lower than in women without this symptom (p = 0.03). Conclusions This study provided no evidence that endothelial function, an early indicator of atherosclerosis, is an important linking factor between insomnia and CHD. Further studies are needed to explore the complex interrelation between sleep and cardiovascular pathology.
Daily egg consumption in hyperlipidemic adults - Effects on endothelial function and cardiovascular risk
Valentine Njike, Zubaida Faridi, Suparna Dutta, Anjelica L Gonzalez-Simon, David L Katz
Nutrition Journal , 2010, DOI: 10.1186/1475-2891-9-28
Abstract: To assess the effects of egg consumption on endothelial function and serum lipids in hyperlipidemic adults.Randomized, placebo-controlled crossover trial of 40 hyperlipidemic adults (24 women, 16 men; average age = 59.9 ± 9.6 years; weight = 76.3 ± 21.8 kilograms; total cholesterol = 244 ± 24 mg/dL). In the acute phase, participants were randomly assigned to one of the two sequences of a single dose of three medium hardboiled eggs and a sausage/cheese breakfast sandwich. In the sustained phase, participants were then randomly assigned to one of the two sequences of two medium hardboiled eggs and 1/2 cup of egg substitute daily for six weeks. Each treatment assignment was separated by a four-week washout period. Outcome measures of interest were endothelial function measured as flow mediated dilatation (FMD) and lipid panel.Single dose egg consumption had no effects on endothelial function as compared to sausage/cheese (0.4 ± 1.9 vs. 0.4 ± 2.4%; p = 0.99). Daily consumption of egg substitute for 6 weeks significantly improved endothelial function as compared to egg (1.0 ± 1.2% vs. -0.1 ± 1.5%; p < 0.01) and lowered serum total cholesterol (-18 ± 18 vs. -5 ± 21 mg/dL; p < 0.01) and LDL (-14 ± 20 vs. -2 ± 19 mg/dL; p = 0.01). Study results (positive or negative) are expressed in terms of change relative to baseline.Egg consumption was found to be non-detrimental to endothelial function and serum lipids in hyperlipidemic adults, while egg substitute consumption was beneficial.As of the early 1970's, a reduction in consumption of eggs, a concentrated source of cholesterol (one yolk provides ~215 mg of cholesterol), had been widely recommended in an effort to lower blood cholesterol and reduce the risk of heart disease[1]. In 1973, the American Heart Association (AHA) guidelines specifically advocated exclusion of eggs from the diet, accompanying the advised cholesterol restriction[2]. More recent AHA guidelines no longer advise for or against egg or egg yolk consumption,
Evaluation of the EndoPAT as a Tool to Assess Endothelial Function  [PDF]
M. Moerland,A. J. Kales,L. Schrier,M. G. J. van Dongen,D. Bradnock,J. Burggraaf
International Journal of Vascular Medicine , 2012, DOI: 10.1155/2012/904141
Abstract: Endothelial dysfunction is a potential target for (pharmaceutical) intervention of several systemic pathological conditions. We investigated the feasibility of the EndoPAT to evaluate acute changes in endothelial function with repeated noninvasive measurements and assessed its discriminating power in different populations. Endothelial function was stable over a longer period of time in renally impaired patients (coefficient of variation 13%). Endothelial function in renally impaired and type 2 diabetic patients was not decreased compared to healthy volunteers ( and , resp., versus , ). The EndoPAT did not detect an effect of robust interventions on endothelial function in healthy volunteers (glucose load: change from baseline , 95% confidence interval ?0.44 to 0.60; smoking: change from baseline , 95% confidence interval ?0.47 to 1.46). This suggests that at present the EndoPAT might not be suitable to assess (changes in) endothelial function in early-phase clinical pharmacology studies. Endothelial function as measured by the EndoPAT could be physiologically different from endothelial function as measured by conventional techniques. This should be investigated carefully before the EndoPAT can be considered a useful tool in drug development or clinical practice. 1. Introduction Endothelial dysfunction is an early predictor of cardiovascular disease [1–3], and might be the causal pathological mechanism of a variety of metabolic diseases, also referred to as the common soil hypothesis [4]. Endothelial function has been shown to be impaired in patients with coronary artery disease, type II diabetes mellitus, hypertension, obesity, renal failure, and hypercholesterolemia [5–9]. It is conceivable that improvement of endothelial function will be an important target in the treatment of these conditions. Therefore, availability of methodology that can be used to reliably assess the effects of (pharmacological) treatments on endothelial function is of critical importance. Endothelial dysfunction is commonly described as the inability of the artery to sufficiently dilate in response to an appropriate endothelial stimulus. It can be assessed by measurement of the arterial pulse wave at a finger artery or by the measurement of flow-mediated dilation (FMD) of the brachial artery after occlusion of the blood flow. Although the exact mechanisms causing FMD are not entirely known, the main mechanism inducing FMD is thought to be an increase in shear stress, leading to the release of nitric oxide from endothelial cells which causes blood vessel dilation [10]. Currently,
Characterisation of Hypertensive Patients with Improved Endothelial Function after Dark Chocolate Consumption  [PDF]
Jenifer d'El-Rei,Ana Rosa Cunha,Adriana Burlá,Marcelo Burlá,Wille Oigman,Mario Fritsch Neves,Agostino Virdis,Fernanda Medeiros
International Journal of Hypertension , 2013, DOI: 10.1155/2013/985087
Abstract: Recent findings indicate an inverse relationship between cardiovascular disease and consumption of flavonoids. We aimed to identify clinical and vascular parameters of treated hypertensive who present beneficial effects of dark chocolate for one-week period on vascular function. Twenty-one hypertensive subjects, aged 40–65?years, were included in a prospective study with measurement of blood pressure (BP), brachial flow-mediated dilatation (FMD), peripheral arterial tonometry, and central hemodynamic parameters. These tests were repeated after seven days of eating dark chocolate 75?g/day. Patients were divided according to the response in FMD: responders ( ) and nonresponders ( ). The responder group presented lower age (54?±?7 versus 61?±?6?years, ), Framingham risk score (FRS) (2.5?±?1.8 versus 8.1?±?5.1%, ), values of peripheral (55?±?9 versus 63?±?5?mmHg, ), and central pulse pressure (PP) (44?±?10 versus 54?±?6?mmHg, ). FMD response showed negative correlation with FRS ( , ), baseline FMD ( , ), baseline reactive hyperemia index (RHI; , ), and central PP ( , ). However, after linear regression analysis, only FRS and baseline RHI were associated with FMD response. In conclusion, one-week dark chocolate intake significantly improved endothelial function and reduced BP in younger hypertensive with impaired endothelial function in spite of lower cardiovascular risk. 1. Introduction Hypertension notably contributes to the worldwide cardiovascular morbidity and mortality. Hypertensive disease seems to have a complex association with endothelial dysfunction, a phenotypical alteration of the vascular endothelium that precedes the development of adverse cardiovascular events and anticipates future cardiovascular risk [1]. Several studies have confirmed the connection between hypertension and abnormal endothelial function in the peripheral, coronary, and renal circulation, suggesting an important mechanism, whereby hypertension promotes the development and progression of vascular disease [1–4]. Given that endothelial dysfunction may be reversible, early detection of this disorder may have therapeutic and prognostic implications [5, 6]. Lifestyle modifications, including dietary habits, have substantial effects on risk factors for cardiovascular disease such as hypertension [7]. Epidemiological evidence demonstrates that a diet rich in fruits and vegetables promotes heart and vascular health [8–10]. These beneficial effects have been largely ascribed to their content in flavonoids. These compounds are synthesized in many edible plants and remain present when
Urinary Leukotriene E4 Is Associated with Renal Function but Not with Endothelial Function in Type 2 Diabetes  [PDF]
Arnar Rafnsson,Magnus B?ck
Disease Markers , 2013, DOI: 10.1155/2013/370461
Abstract: Leukotrienes are inflammatory and vasoactive mediators implicated in endothelium-dependent relaxations and atherosclerosis. Urinary leukotriene E4 (U-LTE4) is a validated disease marker of asthma and increases also in diabetes and acute coronary syndromes. The aim of the present study was to evaluate the association of U-LTE4 and CRP with endothelial function. Urine samples were obtained from 30 subjects (80% males; median age 65) with type 2 diabetes of at least two years duration and a median glomerular filtration rate (eGFR) of 71 (14–129)?mL/min. Reactive hyperemia index (RHI) was used as a measure of microvascular endothelial function, whereas macrovascular endothelial function was determined be means of flow-mediated dilatation of the brachial artery (FMD). Decreased renal function was associated with lower concentrations of U-LTE4. In addition, U-LTE4 was correlated with serum creatinine ( ; ) and eGFR ( ; ). A stepwise multiple linear regression analysis identified eGFR as an independent predictor of U-LTE4 concentrations. In conclusion, the present results did not establish an association of U-LTE4 with endothelial dysfunction. However, eGFR was an independent predictor of U-LTE4, but not CRP, in this cohort, suggesting that GFR should be considered in biomarker studies of U-LTE4. 1. Introduction Urinary concentrations of the lipid-derived mediator leukotriene E4 (U-LTE4) may serve as a disease marker in several pathological conditions, such as asthma [1], obstructive sleep apnea [2], and acute coronary syndromes [3]. In addition, U-LTE4 has been associated with diabetes [4], and U-LTE4 also increases gradually with body mass index (BMI) [2]. In the latter contexts, the leukotriene pathway may not only serve as diagnostic markers but could potentially also offer mechanistic insights into the role of inflammation in metabolic disease. For example, targeting either leukotriene receptor signaling or leukotriene synthesis decreases proinflammatory cytokine secretion from visceral fat [5] and protects against insulin resistance in diet-induced obesity [6, 7]. Importantly, type 2 diabetes is associated with endothelial dysfunction, which plays an important role in the development of vascular complications in these patients [8]. The abnormalities in vascular reactivity associated with type 2 diabetes concern both the micro- and macrocirculation [9]. In the microcirculation, endothelial dysfunction is reflected by reduced extremity skin hyperemia, whereas macrovascular endothelial function can be assessed through brachial artery flow-mediated
Endothelial function and dysfunction: clinical significance and assessment  [cached]
Shaghayegh Haghjooyejavanmard,Mehdi Nematbakhsh
Journal of Research in Medical Sciences , 2008,
Abstract: Over the past two decades, investigators have increasingly recognized the importance of the endothelium as a centralregulator of vascular and body homeostasis. The endothelial lining represents an organ of 1.5 kg in an adult, which is distributed throughout the body. The endothelium is versatile and multifunctional. In addition to its role as a selective permeability barrier, it has many synthetic and metabolic properties, including modulation of vascular tone and blood flow, regulation of immune and inflammatory responses, and regulation of coagulation, fibrinolysis and thrombosis. Endothelial dysfunction (ED) is a frequently used term, which can be referred to abnormalities in various physiological functions of the endothelium, and it is known as a key variable in the pathogenesis of several diseases and their complications. Finding suitable markers for endothelial damage or ED is certainly of interest. Established and emerging techniques to detect ED are divided into three large families of functional, cellular, and biochemical markers. Instead of performing single assessments, it may be much more valuable to determine various biological aspects of endothelium. It seems that there is likely a spectrum between normality, endothelial activation (by inflammatory cytokines), endothelial dysfunction (e.g., impairment of nitric oxide, resulting in loss of regulation of vascular tone) and endothelial damage (e.g., atherosclerosis). In this review we review the importance of endothelium and its activation, biomarkers and dysfunction. KEYWORDS: Endothelial function, endothelium, Disease.
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