Endothelial dysfunction

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The compounds of phenolic nature - new opportunities for pharmacological correction of endothelial dysfunction.

The compounds of phenolic nature - new opportunities for pharmacological correction of endothelial dysfunction.

Previous studies of the metabolism of L-arginine by activated macrophages was found that most of the arginine to urea production is consumed rather than NO, and inhibition of arginase or supplement the culture media with L-arginine led to an increase in nitric oxide synthesis. Furthermore, inhibition of arginase stimulates NO synthesis in endothelial cells. Interestingly, pharmacological inhibition of arginase activity corrects a defect in the NO production in the tissues in diabetes and erectile dysfunction. Therefore, the opportunity is seen preventing conditions data, that is, correction of endothelial dysfunction, underlying, by inhibiting the arginase activity [1, 2, 3]. In recent years, it has been developed and successfully applied the so- called arginase inhibitors - substances of natural origin that can suppress the activity of this enzyme. Furthermore arginase urea production is also involved in the biosynthesis of polyamines, amino acids, ornithine, proline, glutamate. The aim of this study was to conduct a comparative evaluation of pharmacological
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Sonic hedgehog carried by microparticles corrects angiotensin II-induced hypertension and endothelial dysfunction in mice.

Sonic hedgehog carried by microparticles corrects angiotensin II-induced hypertension and endothelial dysfunction in mice.

engineered to over-express different proteins by driving the synthesis of the relevant protein in MP-producing cells [4]. We have demonstrated that MPs released by apoptotic/stimulated human T lymphocytes harbor the morphogen Sonic hedgehog (Shh) and improve endothelial function in the mouse aorta by increasing NO release [5]. Also, endothelial dysfunction in mouse coronary artery after ischemia/reperfusion can be prevented by treatment with Shh-carrying MPs [5]. Moreover, MPs expressing Shh favor in vitro angiogenesis [6] and the recovery of hindlimb flow after peripheral ischemia through the activation of endothelial NO synthase and the increase of NO release and pro-angiogenic factor production [7]. The present study further aims to investigate whether MPs bearing Shh may correct Ang II-induced hypertension and endothelial dysfunction in mice.
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Aerobic Exercise Training Prevents the Onset of Endothelial Dysfunction via Increased Nitric Oxide Bioavailability and Reduced Reactive Oxygen Species in an Experimental Model of Menopause

Aerobic Exercise Training Prevents the Onset of Endothelial Dysfunction via Increased Nitric Oxide Bioavailability and Reduced Reactive Oxygen Species in an Experimental Model of Menopause

Supporting the hypothesis of the present study, 8 weeks of aerobic exercise training was ef- fective in reducing blood pressure and preventing the onset of endothelial dysfunction in ovari- ectomized rats. In fact, the training restored the endothelium-dependent vasodilation induced by ACh in ovarectomized rats, result that is in line with the literature. Figard et al. (2006) [40] showed that isometric strength exercise training contributes to increased endothelium- dependent vasodilation in ovariectomized rats and that this increase in vasodilation is due to greater activation of NOS, cyclooxygenase products, calcium pathways and endothelium- derived hyperpolarizing factors. In addition, Claudio et al (2013) [41] demonstrated that swim- ming training improved coronary vasodilation by enhanced NO bioavailability in ovariecto- mized rats. On the other hand, Pierce et al. (2011) [42] showed that 8 weeks of daily brisk walking was not able to improve the brachial artery flow-mediated dilation in postmenopausal women. Taken together these results suggest that to improve vasodilation in estrogen deficien- cy is necessary prolonged and more intense exercise training.
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Swimming training prevents coronary endothelial dysfunction in ovariectomized spontaneously hypertensive rats

Swimming training prevents coronary endothelial dysfunction in ovariectomized spontaneously hypertensive rats

To assess the role of NO on the vasodilatory re- sponses stimulated by bradykinin, we inhibited the enzyme nitric oxide synthase. A significant reduction in vasodila- tion in all groups was found and the difference between the OVX group and the other groups was maintained. These results suggest that NO plays a key role in the endothelium-dependent vasodilator response even with the estrogen deficiency and that endothelial dysfunction caused by OVX occurs through other mechanisms than the reduction of NO production, such as an increase in oxi- dative stress, which could impair the vasodilation mediated by NO (33,34), prostacyclin (35) and endothelium-derived hyperpolarizing factor (36).
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Implications of maternal nutrient restriction in transgenerational programming of hypertension and endothelial dysfunction across F1-F3 offspring

Implications of maternal nutrient restriction in transgenerational programming of hypertension and endothelial dysfunction across F1-F3 offspring

maternal protein restriction and placental insufficiency have the abil- ity to promote epigenetic programming of the germ line, induction of imprinted-like genes, and subsequent transmission to progeny (Pham et al., 2003; Lillycrop et al., 2005, 2007, 2008; Thompson et al., 2010). In conclusion, our data show that global nutrient restriction during pregnancy results in a specific phenotype that can be passed transgener- ationally to a second and third generation. This transgenerational pheno- type is characterized elevated blood pressure, endothelial dysfunction

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Endothelial Dysfunction and Inflammation Precedes Elevations in Blood Pressure Induced by a High-Fat Diet

Endothelial Dysfunction and Inflammation Precedes Elevations in Blood Pressure Induced by a High-Fat Diet

In conclusion, development of obesity first led to a reduction of endothelial function, which continued to decline over the weeks, and to systemic inflammation, followed by an increase in blood pressure, lipid peroxidation and changes in aortic structure. Our work is relevant in showing the relationship of obesity with chronic inflammation, endothelial dysfunction and hypertension. Despite many studies in this area, the results we found are a further step towards to the development of therapeutic strategies to prevent these abnormalities.

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Endothelial Dysfunction and Pulse Wave Reflection in Women with Polycystic Ovarian Syndrome

Endothelial Dysfunction and Pulse Wave Reflection in Women with Polycystic Ovarian Syndrome

In summary, these PCOS women demonstrated endothelial dysfunction when compared to those young overweight women without the syndrome. Moreover, higher testosterone levels, even in the normal range, were associated with an increase in pulse wave reflection. Large prospective studies are needed to evaluate the prognostic value of FMD, PWV and AIx in this population. In addition, large trials can analyze if measurement of endothelial function and arterial stiffness

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Endothelial Dysfunction and Vitamin D Levels in Kidney Allograft Recipients

Endothelial Dysfunction and Vitamin D Levels in Kidney Allograft Recipients

Before cardiovascular endpoints occur, the patients should have some evidence of early cardiovascular dysfunction. In this regard, markers for endothelial dysfunction may be used as an early inding of cardiovascular disease (28, 29). Endothelial injury is of paramount importance in the development of subsequent cardiovascular complications, and there have been various methods and markers described for the evaluation of endothelial function, including brachial FMD (30), forearm laser Doppler low (31), adhesion molecules (ICAM-1, VCAM-1) (32), von Willebrand factor (33), homocysteine (34), interleukins (35), circulating endothelial cells (36) , and circulating endothelial progenitor cells (37). In recent reports, sTM and sEPCR, important anti-thrombotic factors that are produced extensively by endothelial cells during injury, seem to be markers of endothelial function and in several diseases in which endothelial damage is prominent (38, 39, 40). After binding to EPCR Protein C is activated and shows anti-thrombotic and anti-inlammatory activity. Also, thrombomodulin is a cell surface glycoprotein produced by vascular endothelial cells, is also an important cofactor for activation of protein C. Activated protein C is one of the best known anticoagulants, and it has anti-apoptotic and anti-inlammatory properties (39). Activated protein C, TM and EPCR can be relection of the endothelial response to injury, and recent studies have demonstrated that numerous diseases including sepsis, SLE, Wegener’s granulomatosis, and renal failure were found to be associated with elevated levels of these markers (39, 40). They might also predict the disease activity in Wegener’s granulomatosis. Moreover, renal involvement was associated with higher sEPCR in SLE patients, suggesting that circulating sEPCR may be an indicator of vasculopathy and renal injury in SLE (40). In recent studies, FMD was also
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Endothelial dysfunction in cardiovascular and endocrine-metabolic diseases: an update

Endothelial dysfunction in cardiovascular and endocrine-metabolic diseases: an update

The endothelium plays a vital role in maintaining circulatory homeostasis by the release of relaxing and contracting factors. Any change in this balance may result in a process known as endothelial dysfunction that leads to impaired control of vascular tone and contributes to the pathogenesis of some cardiovascular and endocrine/metabolic diseases. Reduced endothelium- derived nitric oxide (NO) bioavailability and increased production of thromboxane A2, prostaglandin H2 and superoxide anion in conductance and resistance arteries are commonly associated with endothelial dysfunction in hypertensive, diabetic and obese animals, resulting in reduced endothelium-dependent vasodilatation and in increased vasoconstrictor responses. In addition, recent studies have demonstrated the role of enhanced overactivation of β-adrenergic receptors inducing vascular cytokine production and endothelial NO synthase (eNOS) uncoupling that seem to be the mechanisms underlying endothelial dysfunction in hypertension, heart failure and in endocrine-metabolic disorders. However, some adaptive mechanisms can occur in the initial stages of hypertension, such as increased NO production by eNOS. The present review focuses on the role of NO bioavailability, eNOS uncoupling, cyclooxygenase-derived products and pro-inflammatory factors on the endothelial dysfunction that occurs in hypertension, sympathetic hyperactivity, diabetes mellitus, and obesity. These are cardiovascular and endocrine-metabolic diseases of high incidence and mortality around the world, especially in developing countries and endothelial dysfunction contributes to triggering, maintenance and worsening of these pathological situations.
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Maternal biomarkers of endothelial dysfunction and preterm delivery.

Maternal biomarkers of endothelial dysfunction and preterm delivery.

Our purpose was to determine if endothelial dysfunction biomarkers which are known to be linked to CVD risk were also detectable in pregnant women who delivered preterm. This circumstance is analogous to the later risk of type 2 diabetes experienced by women with gestational diabetes. In our prospec- tive nested case-control study of generally healthy pregnant women from Camden, we made three novel and important observations. Firstly, elevated serum levels of the endothelial dysfunction biomarkers sICAM-1 and sVCAM-1 were positively associated with preterm delivery and spontaneous preterm delivery. These associations were independent of confounding by the usual risk factors such as cigarette smoking, preeclampsia and
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High density lipoproteins as indicators of endothelial dysfunction in children with diadetes type I

High density lipoproteins as indicators of endothelial dysfunction in children with diadetes type I

The aim of the investigation was to study the level of blood high density lipoproteins (HDL) in the groups of children with different course of diadetes type I in order to find out the dependence of course and complications of diabetes on that level. Materials and methods: Blood high density lipoprotein (HDL) levels were investigated in children and adoles- cents with diadetes type I, depending on the duration of diadetes type I, age, stage of sexual development, the stage of diabetic nephropathy and levels of plasma endothelin-1 (E-1). Results: Decrease in HDL level with increasing duration of diadetes type I in prepubertate patients, higher indices of HDL cholesterol were determined in girls, especially with impaired puberty. HDL cholesterol was higher in diabetic nephropathy at the stage of proteinuria and high level of blood endothelin-1. Conclusion: The revealed changes were considered to cause deregulation of vascular endothelium as a manifestation of the initial stages of endothelial dysfunction.
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Mechanisms of reperfusion-induced coronary endothelial dysfunction

Mechanisms of reperfusion-induced coronary endothelial dysfunction

The observation that the reintroduction of molecular oxygen at reperfusion is re- quired to produce postischemic endothelial dysfunction is consistent with the view that ischemia/reperfusion injury to the endothe- lium may result from the generation of reac- tive oxygen species. This has now been clearly demonstrated by the observation that endothelial dysfunction can be attenuated or prevented by scavengers of these species. In our rat model of myocardial ischemia/reper- fusion, a continuous intravenous infusion of the free radical scavenger N-2-mercaptopro- pionyl glycine (MPG) during ischemia and reperfusion resulted in the prevention of the coronary endothelium-dependent relaxation in response to acetylcholine (9). There is also evidence in species other than rats that the reperfusion-induced endothelial injury is the consequence of the production of oxy- gen-derived free radicals because impaired endothelium-dependent relaxation can be restored by treatment with superoxide dis- mutase and catalase in both large coronary arteries (4,10) and the microcirculation (11). Several mechanisms may explain the en- dothelial injury induced by free radicals. Once produced, superoxide anions may di- rectly inactivate NO (12,13). Since NO is a potent inhibitor of neutrophil activation and adhesion (14), the decreased NO production may lead to the development of an acute inflammatory response. Moreover, since free radicals produced during reperfusion also trigger the rapid adhesion of neutrophils to endothelial cells through the induction of
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Low vaspin levels are related to endothelial dysfunction in patients with ankylosing spondylitis

Low vaspin levels are related to endothelial dysfunction in patients with ankylosing spondylitis

vaspin levels. They found an independent association between serum vaspin levels and intima-media thickness. Moreover, previous works have suggested that low vaspin emerged as an important factor for coronary artery disease (28). Endothelial dysfunction is one of the first signs of atherosclerosis and cardiovascular diseases. Brachial FMD has been a widely used noninvasive method for the assessment of vascular endothelial function. Many clinical studies showed that ankylosing spondylitis is associated with vascular endothelial dys- function, which leads to accelerated atherosclerosis. However, few studies have evaluated the association of vaspin with endothelial function in patients with ankylosing spondylitis. The present study found that vaspin was asso- ciated with endothelial function, in which serum vaspin levels in patients increased gradually as FMD levels increased from quartile 1 to quartile 4 (Table 2).
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Endothelial Dysfunction and Pulse Wave Reflection in Women with Polycystic Ovarian Syndrome

Endothelial Dysfunction and Pulse Wave Reflection in Women with Polycystic Ovarian Syndrome

In summary, these PCOS women demonstrated endothelial dysfunction when compared to those young overweight women without the syndrome. Moreover, higher testosterone levels, even in the normal range, were associated with an increase in pulse wave reflection. Large prospective studies are needed to evaluate the prognostic value of FMD, PWV and AIx in this population. In addition, large trials can analyze if measurement of endothelial function and arterial stiffness

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Mechanisms of endothelial dysfunction in resistance arteries from patients with end-stage renal disease.

Mechanisms of endothelial dysfunction in resistance arteries from patients with end-stage renal disease.

The study focuses on the mechanisms of endothelial dysfunction in the uremic milieu. Subcutaneous resistance arteries from 35 end-stage renal disease (ESRD) patients and 28 matched controls were studied ex-vivo. Basal and receptor- dependent effects of endothelium-derived factors, expression of endothelial NO synthase (eNOS), prerequisites for myoendothelial gap junctions (MEGJ), and associations between endothelium-dependent responses and plasma levels of endothelial dysfunction markers were assessed. The contribution of endothelium-derived hyperpolarizing factor (EDHF) to endothelium-dependent relaxation was impaired in uremic arteries after stimulation with bradykinin, but not acetylcholine, reflecting the agonist-specific differences. Diminished vasodilator influences of the endothelium on basal tone and enhanced plasma levels of asymmetrical dimethyl L-arginine (ADMA) suggest impairment in NO-mediated regulation of uremic arteries. eNOS expression and contribution of MEGJs to EDHF type responses were unaltered. Plasma levels of ADMA were negatively associated with endothelium-dependent responses in uremic arteries. Preserved responses of smooth muscle to pinacidil and NO-donor indicate alterations within the endothelium and tolerance of vasodilator mechanisms to the uremic retention products at the level of smooth muscle. We conclude that both EDHF and NO pathways that control resistance artery tone are impaired in the uremic milieu. For the first time, we validate the alterations in EDHF type responses linked to kinin receptors in ESRD patients. The association between plasma ADMA concentrations and endothelial function in uremic resistance vasculature may have diagnostic and future therapeutic implications.
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Obesity: Paradigm of Endothelial Dysfunction in Paediatric Age Groups

Obesity: Paradigm of Endothelial Dysfunction in Paediatric Age Groups

Material and Methods: Approximately 10% of the world’s paediatric population has excess weight or obesity and 40% of these will be obese adults. Obesity is characterized by a chronic, low grade, pro-inflammatory process that ultimately results in endothelial dysfunc- tion, the trigger lesion leading to adult cardiovascular disease. This leads to an imbalance in the synthesis of mediators that normally regulate vascular homeostasis, particularly nitric oxide bioavailability, favoring a pro-atherosclerotic status, the hallmark of cardiovas- cular disorders.

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A novel genetic score approach using instruments to investigate interactions between pathways and environment: application to air pollution.

A novel genetic score approach using instruments to investigate interactions between pathways and environment: application to air pollution.

through the generation of oxygen-centered free radicals that reduce the bioavailability of endothelium-derived NO without prior interaction with the lung or vascular tissue [38]. These two interconnected mechanisms could explain why we observed associations between black carbon and fibrinogen only among individuals with high genetic risk profiles related to oxidative stress and endothelial function. The endothelium is the layer of epithelial cells that lines the cavities of the heart, blood, lymph vessels, and the serous cavities of the body. Impaired endothelial function leads to impaired control of blood pressure, inflammation, formation of new blood vessels, and blood clotting [39]. Endothelial dysfunction is considered as a key early event in the development of atherosclerosis [1]. A high endothelial dysfunction score, repre- senting a higher allelic risk profile, may therefore identify a subset of participants having stronger coagulation responses to traffic- related air pollution.
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J. Bras. Nefrol.  vol.37 número1

J. Bras. Nefrol. vol.37 número1

It is well recognized that oxidation of the cofactor tetrahydrobiopterin (BH 4 ) to BH 2 provides an important contribution to eNOS uncoupling. Interestingly, BH 4 supplementation abolished elevated superoxide production in SHR. This finding indicates that vascular oxidative stress contributes to endothelial dysfunction and hypertension by uncoupling eNOS, and possibly by oxidation of BH 4 . It has been reported that BH 4 supplementation starting at an early age (5-16 weeks of age) suppressed the development of hypertension in SHR. 46 Furthermore,

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(São Paulo, online)  vol.1 número5

(São Paulo, online) vol.1 número5

BACKGROUND: The high prevalence of obesity in the world is associated with several health problems, with endothelial dysfunction iguring as a frequent feature.We investigated whether low dose consumption of green tea extract (catechins,< 200 mg/day) could modify endothelial function, lipid proile, fasting glucose and insulin, post load plasma glucose, inlammatory/oxidative stress biomarkers and blood pressure in obese women.

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