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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The author describes some of the numerous domains regarding the new topic called "Vascular endothelial dysfunction, oxidative stress". The endothelium is responsible for the constancy and integrity of the milieu interieur by producing various substances. Endothelial dysfunction occurs when there is imbalance between vasodilators and vasoconstrictors, growth factors and their inhibitors, proinflammatory and antiinflammatory agents, prothrombotic and fibrinolytic activities. The reason for this imbalance may be response to vascular endothelial or intimal injury caused by mechanical, physical, chemical, microbiological, immunologic, genetic damage or any of their combination. Endothelial dysfunction occurring on the huge inner surface of the vessels (the endothelium) is responsible for the triggering of atherosclerosis, which is a chronic vascular disease. All the risk factors of vascular pathology are leading to chronic (cardio)vascular diseases by causing endothelial dysfunction. Decreased endogenous antioxidative capacity leads to oxidative stress by free radical reactions of physiological oxidative metabolic processes, ending as the ultimate reason for endothelial dysfunction induced by risk factors. The therapeutic and preventive effects of causal antioxidant treatments having intracellular and mitochondrial effects (statins, angiotensin-converting-enzyme inhibitors, angiotensin-receptor-blockers, acetylsalicylic acid, and third generation beta-blockers) should be emphasized. It is also important to underline the physiological-pathophysiological-therapeutic consubstantiality and systemic nature of human vasculature and to emphasize the preventive-therapeutic significance of the vascular consequence cascade. And finally, there has been large process in the assessment of oxidative stress and consecutive endothelial dysfunction which revolutionized our clinical point of view.
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PMID:[Vascular endothelial dysfunction, oxidative stress--a new topic within the referral section of Orvosi Hetilap]. 1861 60

It is now two decades since it was demonstrated that ET-1 is one of the most powerful vasoconstrictors in biology. ET-1 mediates its effects through two membrane G-protein coupled receptors, ET(A) and ET(B), which exhibit a wide tissue distribution including the endothelial cells, vascular smooth muscle cells and adventitial fibroblasts. In recent years, ET-1 has been identified as a key player of endothelial dysfunction in various cardiovascular, autoimmune and CTDs. Endothelial dysfunction results from endothelial cell injury subsequently leading to the generation of an inflammatory process and endothelial cell activation. Thus, beyond its known 'classical' vasoactive effects, ET-1 is additionally considered to be an important mediator in vessel remodelling ultimately leading to major changes in cellular and tissue architecture; it also appears to function in conjunction with other growth factors and cytokines. Consequently, ET-1 receptor antagonists may be useful in ameliorating progression of vascular dysfunction and vascular disease due to their ability to negatively modulate vasoconstrictor pathways, cytokines and inflammatory markers production, and growth factor effects. This review briefly summarizes the current knowledge on the role of ETs in vascular dysfunction and vascular disease, with a particular emphasis on ET-1 in CTDs.
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PMID:Endothelin--role in vascular disease. 1878 33

Endothelial dysfunction is an important process in the development of atherosclerotic cardiovascular disease, while it is also a major pathophysiological mechanism underlying vasculogenic erectile dysfunction (ED). Expectedly, these two prevalent disorders are linked also at the clinical level: ED is common in patients with overt and silent coronary artery disease, while ED is increasingly being regarded as the early clinical manifestation of a generalized vascular disease and carries an independent risk for future cardiovascular events. The emerging awareness of ED as a barometer for cardiovascular disease offers a unique opportunity to enhance preventive vascular health in men. Lifestyle and risk factor modification, as well as pharmacologic therapy (both phosphodiesterase type-5 inhibitors and non-ED-targeting drugs), appear to confer additional benefit both in terms of ED treatment and overall cardiovascular risk; this benefit may be related, at least partly, to the improvement of endothelial function and anti-inflammatory effects. The present review identifies pathophysiologic links between endothelial dysfunction, ED and coronary artery disease, presents methodological aspects regarding penile and systemic endothelial function, and discusses the clinical implications in terms of diagnosis of ED, assessment of patient risk, and treatment.
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PMID:The triad: erectile dysfunction--endothelial dysfunction--cardiovascular disease. 1912 23

Endothelial dysfunction (EtD) has emerged as a critical master pathway in the pathogenesis of both vascular disease and erectile dysfunction (ED). Drugs that have been developed for vascular diseases and/or found to have beneficial endothelial effects may be helpful in the management of ED. In this manuscript we summarize the current state of the art with respect to endothelial active drugs and discuss the evidence supporting their use in the management of ED. Pubmed query for the terms Endothelial dysfunction, erectile dysfunction, pharmaceuticals, "endothelium", "function", "pharmaceutical", "eNOS", "erectile dysfunction" and "erectile function" was conducted. Relevant articles were reviewed and summarized. A variety of cardiovascular medications have mechanisms of action that involve the endothelium. Examples include HMG-CoA Reductase inhibitors ("statins"), Angiotensin Converting Enzyme Inhibitors (ACEI), Angiotensin Receptor blockers (ARB), Endothelin Receptor Antagonists (ERA), certain beta blockers, and some oral hypoglycemics. Some of these drugs have been found to improve penile erection, although an endothelium dependent mechanism has not been conclusively demonstrated in all studies. Drugs that improve endothelial function in the cavernous arteries and the erectile tissues of the corpora cavernosa hold great promise in treating or at least minimizing the vascular damage that contributes to ED. ACEI and ARB appear to hold great promise in this regard, while statins and oral hypoglycemics may play a potentially useful role as adjunctive therapy for ED. Improvements in endothelial function may help reverse ED in some cases, which would be a marked improvement over management with currently available "on demand" ED therapies.
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PMID:Drugs designed to improve endothelial function: effects on erectile dysfunction. 1912 28

Endothelial dysfunction is a characteristic of aging-related vascular disease and is worsened during diabetes. High glucose can impair endothelial cell (EC) function through cellular accumulation of reactive oxygen species, an insult that can also limit replicative lifespan. Nicotinamide phosphoribosyltransferase (Nampt), also known as PBEF and visfatin, is rate-limiting for NAD+ salvage from nicotinamide and confers resistance to oxidative stress via SIRT1. We therefore sought to determine if Nampt expression could resist the detrimental effects of high glucose and confer a survival advantage to human vascular EC in this pathologic environment. Human aortic EC were infected with retrovirus encoding eGFP or eGFP-Nampt, and FACS-selected to yield populations with similar, modest transgene expression. Using a chronic glucose exposure model we tracked EC populations to senescence, assessed cellular metabolism, and determined in vitro angiogenic function. Overexpression of Nampt increased proliferation and extended replicative lifespan, and did so preferentially during glucose overload. Nampt expression delayed markers of senescence and limited reactive oxygen species accumulation in high glucose through a modest increase in aerobic glycolysis. Furthermore, tube networks formed by Nampt-overexpressing EC were more extensive and glucose-resistant, in accordance with SIRT1-mediated repression of the anti-angiogenic transcription factor, FoxO1. We conclude that Nampt enables proliferating human EC to resist the oxidative stress of aging and of high glucose, and to productively use excess glucose to support replicative longevity and angiogenic activity. Enhancing endothelial Nampt activity may thus be beneficial in scenarios requiring EC-based vascular repair and regeneration during aging and hyperglycemia, such as atherosclerosis and diabetes-related vascular disease.
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PMID:Nicotinamide phosphoribosyltransferase imparts human endothelial cells with extended replicative lifespan and enhanced angiogenic capacity in a high glucose environment. 1930 75

Endothelial dysfunction is a fundamental step in the atherosclerotic disease process. Its presence is a risk factor for the development of clinical events, and may represent a marker of atherothrombotic burden. Also, endothelial dysfunction contributes to enhanced plaque vulnerability, may trigger plaque rupture, and favors thrombus formation. The assessment of endothelial vasomotion is a useful marker of atherosclerotic vascular disease. There are different methods to assess endothelial function: endothelium-dependent vasodilatation brachial flow-mediated dilation, cerebrovascular reactivity to L-arginine, and the determination of some biomarkers such as microalbuminuria, platelet function, and C-reactive protein. Endothelial dysfunction has been observed in stroke patients and has been related to stroke physiopathology, stroke subtypes, clinical severity and outcome. Resting ankle-brachial index (ABI) is also considered an indicator of generalized atherosclerosis, and a low ABI is associated with an increase in stroke incidence in the elderly. Despite all these data, there are no studies analyzing the predictive value of ABI for new cardiovascular events in patients after suffering an acute ischemic stroke. ARTICO is an ongoing prospective, observational, multicenter study being performed in 50 Spanish hospitals. The aim of the ARTICO study is to evaluate the prognostic value of a pathological ABI (<or=0.9) in the presence of a major cardiovascular event during a 1-year follow-up after first-ever ischemic stroke. Secondary objectives include the evaluation of the predictive value for major cardiovascular events of the carotid intima-media thickness, carotid duplex findings, and certain biomarkers. Data from the ARTICO study will increase the knowledge of patient outcome after ischemic stroke and may help to improve our ability to detect patients at high risk of stroke recurrence or major cardiovascular events.
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PMID:Endothelial dysfunction, vascular disease and stroke: the ARTICO study. 1934 31

Endothelial dysfunction secondary to persistent hyperglycemia plays a key role in the development of type 2 diabetic vascular disease. The aim of the present study was to examine the protective effect of resveratrol against hyperglycemia-induced endothelial dysfunction. In cultured human umbilical vein endothelial cells (HUVECs), resveratrol (10-100 microM) concentration dependently enhanced phosphorylation of endothelial nitric oxide synthesis (eNOS) at Ser1177 and nitric oxide (NO) production. In addition, resveratrol can increase the phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) at Thr172 and suppress high glucose-induced generation of superoxide anion. In mouse aortic rings, resveratrol (1-100 microM) elicited endothelium-dependent vasodilatations and alleviated high glucose-mediated endothelial dysfunction. All these beneficial effects of resveratrol on the endothelium were abolished by pharmacological antagonism of AMPK by compound C. These results provide new insight into the protective properties of resveratrol against endothelial dysfunction caused by high glucose, which is attributed to the AMPK mediated reduction of superoxide level.
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PMID:Resveratrol prevents hyperglycemia-induced endothelial dysfunction via activation of adenosine monophosphate-activated protein kinase. 1966 1

Epidemiological studies suggests that migraine is associated with disorders of the cerebral, coronary, retinal, dermal and peripheral vasculature. There is evidence that migraine is associated with endothelial dysfunction, both as a cause and a consequence. Endothelial dysfunction, a vascular risk factor, is characterized by endothelial activation and impaired vascular reactivity. Plasma and genetic biomarkers for these conditions have been identified. The clinical significance lies in the potential for the rapid identification of migraineurs at increased risk of ischaemic stroke and vascular disease through ascertainment of endothelial dysfunction biomarkers. It is uncertain whether stroke, myocardial infarction and other vasculopathies can be prevented by migraine prophylaxis, endothelial repair, platelet inhibition or a combination of these strategies.
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PMID:Migraine as a systemic vasculopathy. 1968 7

Obesity is associated with a high prevalence of erectile dysfunction; however, the pathophysiological link between obesity and erectile dysfunction remains poorly understood. In this minireview, we have attempted to evaluate the existing literature pertaining to obesity and erectile dysfunction to determine whether a common pathophysiological link exists. Visceral obesity is associated with increased inflammatory responses, which contribute to endothelial dysfunction. Furthermore, obesity is also associated with reduced plasma testosterone levels, which contributes to hypogonadism and increases the risk of vascular pathology. Endothelial dysfunction and androgen deficiency have previously been linked to the pathophysiological mechanisms of erectile dysfunction. The underlying pathophysiological mechanisms of endothelial dysfunction and testosterone deficiency include penile vascular insufficiency as a result of the loss of nitric oxide synthase expression and activity and the loss of tissue compliance, resulting in reduced hemodynamic properties. Recent progress in the field of sexual medicine has recognized the impact of vascular disease and hypogonadism on the management of patients with erectile dysfunction. We suggest that visceral obesity, a component of the metabolic syndrome, adversely affects endothelial function and testosterone levels, contributing to hypogandism and erectile dysfunction. Thus, clinical screening for the risk of erectile dysfunction in obese patients should include the assessment of waist circumference, testosterone levels, body mass index and physical inactivity.
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PMID:Mechanisms of obesity and related pathologies: androgen deficiency and endothelial dysfunction may be the link between obesity and erectile dysfunction. 1975 71

Diabetes mellitus is becoming increasingly prevalent and magnifies the risk of cardiovascular complications. Endothelial dysfunction caused by oxidative stress is a hallmark of diabetes and is responsible for the ubiquitous manifestations of vascular disease in diabetics. Compared with non-diabetic patients, coronary artery disease is more severe and the clinical outcome impaired in diabetic patients undergoing revascularisation. Despite these limitations the benefit of revascularisation therapy is particularly pronounced in diabetics. The optimal revascularisation strategy (coronary artery bypass graft surgery versus percutaneous coronary intervention) in diabetic patients with coronary artery disease depends on clinical and anatomical considerations.
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PMID:Revascularisation of coronary artery disease in patients with diabetes mellitus. 1995 32


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