Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endothelial dysfunction is considered in the paper from the point of view of pathology of cellular membranes presenting as vesiculation of cytoplasmatic membrane, release of membrane-bound microparticles, elevation of concentration of peeled off endotheliocytes in the blood. Comparative analysis of action of angiotensin converting enzyme inhibitors with various affinities to tissue renin-angiotensin-aldosterone system on the indicated parameters of pathology of cellular membranes and endothelial dysfunction has been conducted. The following mechanisms of stabilization of membranous homeostasis under influence of angiotensin converting enzyme inhibitor perindopril are discussed: action on apoptosis and activation of cells.
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PMID:[Pronounced homeostatic action of angiotensin converting enzyme inhibitors with high affinity to tissue renin-angiotensin-aldosterone system on cellular membranes]. 1826 Sep 12

Endothelial dysfunction crucially contributes to the development of impaired coronary and systemic perfusion as well as reduced exercise capacity in patients with congestive heart failure, with fundamental impact on morbidity and mortality. Reduced bioavailability of nitric oxide (NO) and abundant formation of reactive oxygen species (ROS) within the vascular wall are the key determinants in endothelial dysfunction. The imbalance between NO and ROS mainly results from neurohumoral activation associated with heart failure. As endothelial derived NO is a major endogenous modulator of platelet function, reduced intravascular bioactivity of NO contributes to platelet activation, adhesion and thromboembolic events in heart failure. Treatment with angiotensin converting enzyme (ACE) inhibitors, angiotensin and aldosterone antagonists, and statins beneficially modulates endothelial dysfunction in heart failure. All these therapies increase NO bioactivity by either modulation of ROS generation, thereby preventing the interaction of superoxide anions with NO, and/or increasing endothelial NO synthase (eNOS) expression/activity. AVE9488, a novel eNOS transcription enhancer, attenuates cardiac remodeling and endothelial dysfunction in rats after large myocardial infarction. Endothelial progenitor cell (EPC) levels and their mobilization are regulated by eNOS. After myocardial infarction in rats, EPC levels and formation of endothelial colony forming units are markedly reduced. AVE 9488, ACE or HMG-CoA reductase inhibition result in significant increases in EPC levels, and beneficial effects on bone marrow molecular alterations after myocardial infarction.
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PMID:Endothelial dysfunction in heart failure. 1827 93

1. Epidemiological aspects: There is evidence that the pandemic of DM is entering a stabilization phase, with a slight downturn in the rates of ESRD attributed to DM in the United States. 2. New pathogenic and progression mechanisms of renal disease are proposed: 1) Intraglomerular hyperpressure with phenotypical cell changes, inducing TGF-beta activation; 2) Genetic polymorphisms, with candidate genes in chromosomes 18q, 3q, 7p and others; 3) Endothelial dysfunction as an injury initiating mechanism, demonstrated in the eNOS knockout rat; 4) Isoforms of PKC molecules that favor progression of nephropathy. 3. Importance of metabolic syndrome as a progression factor of chronic renal disease. 4. Increased CV risk in patients treated with thiazolidinediones (glitazones) -Hydrosaline retention and heart failure. 5. Recent studies: ADVANCE study: Combined treatment with an ACE inhibitor (perindropil) and a diuretic (indapamide) in fixed doses helps to reduce CV risk and overall mortality.DREAM study: Ramipril does not reduce the occurrence of DM2, but does improve reversion to normoglycemia. AVOID study: Direct renin inhibitors add greater antihypertensive and antiproteinuric efficacy. 6. New therapeutic targets: Antifibrotic, anti-inflammatory and antiproteinuric effects of sulodexide, isosorbide mononitrate, PKC inhibitors and others. 7. The most effective strategy continues to be intensive, multifactorial and multidisciplinary management of the type 2 diabetic patient, as shown by long-term follow-up in the Steno-2 study.
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PMID:[Advances in diabetes mellitus, diabetic nephropathy, metabolic syndrome and cardio-vascular-renal risk]. 1884 25

Endothelial dysfunction, which is defined by decreased endothelium-dependent vasodilatation, is associated with an increased number of cardiovascular events. Nitric oxide (NO) bioavailability is reduced by altered endothelial signal transduction or increased formation of radical oxygen species reacting with NO. Endothelial dysfunction is therapeutically reversible and physical exercise, calcium channel blockers, angiotensin converting enzyme inhibitors, and angiotensin receptor antagonists improve flow-evoked endothelium-dependent vasodilation in patients with hypertension and diabetes. We have investigated three different approaches, with the aim of correcting endothelial dysfunction in cardiovascular disease. Thus, (1) we evaluated the effect of a cell permeable superoxide dismutase mimetic, tempol, on endothelial dysfunction in small arteries exposed to high pressure, (2) investigated the endothelial signal transduction pathways involved in vasorelaxation and NO release induced by an olive oil component, oleanolic acid, and (3) investigated the role of calcium-activated K channels in the release of NO induced by receptor activation. Tempol increases endothelium-dependent vasodilatation in arteries from hypertensive animals most likely through the lowering of radical oxygen species, but other mechanisms also appear to contribute to the effect. While oleanolic acid leads to the release of NO by calcium-independent phosphorylation of endothelial NO synthase, endothelial calcium-activated K channels and an influx of calcium play an important role in G-protein coupled receptor-evoked release of NO. Thus, all three approaches increase bioavailability of NO in the vascular wall, but it remains to be addressed whether these actions have any direct benefit at a clinical level.
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PMID:Novel approaches to improving endothelium-dependent nitric oxide-mediated vasodilatation. 1930 98

Endothelial damage, with loss of the vascular protective effects of nitric oxide (NO), is an important early step in the development of microvascular and macrovascular complications of diabetes. Endothelial dysfunction is closely associated with diabetic nephropathy in type 1 and 2 diabetes. In this review we will discuss the mechanisms by which hyperglycemia may cause kidney damage and endothelial dysfunction. Hyperglycemia causes microvascular dysfunction, which contributes to the development of end stage renal disease. Determining the role of endothelial abnormalities in the development of diabetic nephropathy is critical to understanding the etiology and pathogenesis of the microvascular complications of diabetes. Endothelial function can be assessed by invasive and noninvasive techniques both in the coronary and peripheral circulation. Endothelial dysfunction is considered a reversible phenomenon; pharmacological intervention with hypolipidemic agents, insulin sensitizers, ACE inhibitors and angiotensin II receptor blockers (ARB) as well as dietary and lifestyle modifications have been shown to reverse it.
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PMID:[Endothelial dysfunction and diabetes: possible role in kidney damage]. 1964 21

Endothelial dysfunction is characterized by an impairment of endothelium-dependent vasodilatation. It has been linked to each of the known atherogenic risk factors, including diabetes mellitus, hypertension, dyslipidaemia, cigarette smoking, menopause, etc. A number of recent studies have shown that the severity of endothelial dysfunction correlates with the development of coronary artery disease and predicts future cardiovascular events. Therefore, these findings strengthen the hypothesis that endothelial dysfunction may be an early stage of coronary atherosclerosis. This phenomenon primarily reflects an imbalance between the vasodilating (nitric oxide) and vasoconstrictor agents (endothelin-1). Several invasive (intracoronary or intrabrachial infusions of vasoacting agents) and non-invasive techniques (assessment of flow mediated vasodilatation in the brachial artery by ultrasound) have been developed during the last few years to evaluate endothelial function in the coronary and peripheral circulation. This new methodology has allowed assessing the severity of the abnormalities in vascular function and their regression by several pharmacological and non-pharmacological interventions. It is likely that restoration of endothelial function can regress the atherosclerotic disease process and prevent future cardiovascular events. Most pharmacological interventions attempting to improve endothelial dysfunction targeted the risk factors linked to endothelial dysfunction: hypertension (ACE-inhibitors, calcium antagonists), dyslipidaemia (lipid-lowering agents) and menopause (estrogens). Nevertheless, several pharmacological agents have been suggested to achieve vascular protection through different mechanisms beyond their primary therapeutic actions: ACE-inhibitors, statins, third generation of beta-blockers (nebivolol), endothelium-derived nitric oxide synthesis (tetrahydrobiopterin, BH4) and antioxidants agents. In this review we will focus on the current pharmacological management of the endothelial dysfunction.
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PMID:Current pharmacological approach to restore endothelial dysfunction. 1968 60

Vascular endothelium is not simply a barrier between blood and extra vascular bed but is a source of large number of mediators regulating various functions of the body among which nitrous oxide appears to be one of most important. Endothelial dysfunction (ED) develops in a number of processes: diabetes mellitus, smoking, arterial hypertension, hypercholesterolemia. ED promotes increase of rate development of cardiovascular diseases. One of most well known markers of ED is microalbuminuria (MAU). Drug and nondrug means are used for the treatment of ED. Calcium antagonists and angiotensin converting enzyme inhibitors both separately and as components of combination therapy are able to maximally diminish MAU.
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PMID:[Value of endothelial dysfunction in cardiovascular diseases and methods of its correction with drugs]. 2083 Oct 49

Nitric oxide (NO) is a soluble gas continuously synthesized from the amino acid L-arginine in endothelial cells by the constitutive calcium-calmodulin-dependent enzyme nitric oxide synthase (NOS). Endothelial dysfunction has been identified as a major mechanism involved in all the stages of atherogenesis. Evaluation of endothelial function seems to have a predictive role in humans, and therapeutic interventions improving nitric oxide bioavailability in the vasculature, may improve the long-term outcome in healthy individuals, high-risk subjects or patients with advanced atherosclerosis. Several therapeutic strategies (including statins, angiotensin converting enzyme inhibitors/angiotensin receptors blockers, insulin sensitizers, antioxidant compounds) are now available, targeting both the synthesis and oxidative inactivation of NO in human vasculature, reversing in that way endothelial dysfunction which is enhanced by the release of nitric oxide from the endothelium.
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PMID:Novel agents targeting nitric oxide. 2211 48

A large body of evidence indicates that patients with essential hypertension are characterized by endothelial dysfunction mediated by an impaired NO availability secondary to oxidative stress production. A dysfunctioning endothelium is an early marker of the development of atherosclerotic changes and can also contribute to cardiovascular events. Vascular reactivity tests represent the most widely used methods in the clinical assessment of endothelial function. In the last two decades, many studies have evaluated the endothelium in hypertensive patients, using different techniques. Several methodologies were developed to study microcirculation (resistance arteries and arterioles) and macrocirculation (conduit arteries), both in coronary and peripheral vascular districts. This review will describe the most relevant available techniques in the research on endothelial dysfunction in essential hypertension, their advantages and limitations, focusing on available data on endothelial dysfunction and on the effect of treatment. Endothelial dysfunction in the coronary and peripheral circulation of hypertensive patients are associated with hypertensive target organ damage and it is predictive of cardiovascular events. Several non-pharmacological approaches, including physical exercise and dietary interventions, can ameliorate endothelial function in hypertensive patients. Despite blood pressure reduction per se is not effective, some antihypertensive drugs can improve endothelial dysfunction, particularly calcium channel antagonist in the microcirculation, ACE-inhibitors and AT1-receptor antagonists mostly in conduit arteries. Some beneficial effects were also exerted by nebivolol and statins. Future studies are needed to confirm whether the improvement in endothelial dysfunction is associated to better cardiovascular prognosis in hypertension.
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PMID:Hypertension and endothelial dysfunction: therapeutic approach. 2211 51

Endothelial dysfunction is found in hypertensive patients and may serve as a prognostic marker of future cardiovascular events. Endothelial function can be assessed noninvasively by flow-mediated vasodilation (FMD). The goal of this paper is to summarize comprehensively the clinical trials that investigated the effects of antihypertensive drugs on endothelial function assessed by FMD in hypertensive patients. A PubMed-based search found 38 clinical trial papers published from January 1999 to June 2011. Significant improvement of FMD after antihypertensive treatment was shown in 43 of 71 interventions (among 38 clinical trial papers). Angiotensin II receptor blockers and angiotensin converting enzyme inhibitors appeared to improve FMD more than other drug types. Antihypertensive treatment can improve endothelial dysfunction when assessed by FMD, although there are conflicting data that require further research.
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PMID:The effect of antihypertensive drugs on endothelial function as assessed by flow-mediated vasodilation in hypertensive patients. 2248 72


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