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

---

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

The role of the endothelium in human disease recently has become the focus of intense scientific investigation. Impaired endothelial function is associated with a number of disease states, including cardiovascular disease (CVD) and its major risk factors. Endothelial dysfunction precedes overt vascular disease by years and may itself be a potentially modifiable CVD risk factor. Although no gold standard for the measurement of endothelial function exists, the measurement of flow-mediated dilation (FMD) in the brachial artery, assessed with Doppler ultrasonography, is the most studied method and shows the most promise for clinical application. It is a well-tolerated, noninvasive, and low-risk procedure. Brachial artery FMD after transient vascular occlusion may serve as an index of nitric oxide bioavailability, and its impairment correlates with coronary arterial abnormalities. These factors, with the wide availability of vascular ultrasound scanning in clinical practice, make brachial artery FMD an attractive screening tool for endothelial dysfunction. Present limitations of this procedure include the lack of a consensus definition of normal FMD and the variability among centers in both procedural technique and image analysis. However, these limitations are likely to be overcome with increasing experience and advances in technology, and with further refinements, the measurement of brachial artery FMD will likely become the clinical technique of choice for the evaluation of endothelial disease.
...
PMID:Detection of endothelial dysfunction with brachial artery ultrasound scanning. 1279 48

Cardiovascular disease is a leading cause of death and disability in patients with diabetes or metabolic syndrome (MS). The available data suggest that many patients with diabetes or MS already have vascular abnormalities by the time they are diagnosed with their metabolic disorder. Endothelial dysfunction (ED), which is one of the initial steps in the process of vascular disease, is often present in patients with diabetes or MS. Although the precise mechanism(s) by which diabetes or MS causes ED remains to be elucidated, several possibilities exist. Hyperglycemia, hyperinsulinemia, increased oxidative stress, and diabetic dyslipidemia can all contribute to ED individually or in concert with one another. ED in the setting of diabetes or MS can subsequently result in the activation of a variety of pathways that alter vascular function and participate in the process of vascular remodeling and atherosclerosis. Because insulin resistance is the predominant mechanism responsible for various perturbations seen in MS or diabetes, it is essential to develop a therapeutic strategy that can improve insulin sensitivity with the hope that such interventions would reduce the risk of future cardiovascular events.
...
PMID:Mechanisms of endothelial dysfunction in the metabolic syndrome. 1286 90

Vascular risk factors increase the risk of developing Alzheimer's disease. Increased concentrations of circulating homocysteine are associated with an increased risk of both vascular disease and Alzheimer's disease. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase. There is an increase in the concentration of ADMA in the circulation in vascular disease. We measured the concentrations of homocysteine, ADMA and nitric oxide (as nitrate and nitrite) in the plasma of 25 patients with Alzheimer's disease and 25 control subjects. There was a highly significant increase in the plasma concentration of homocysteine (P<0.001) and ADMA (P<0.0001) and a highly significant decrease in the plasma concentration of nitric oxide (P<0.0001) among the Alzheimer's patients. In the combined patient and control groups a highly significant positive correlation was found between the plasma concentrations of homocysteine and ADMA (r=0.782, P<0.0001). In addition, significant negative correlations were detected between the plasma concentration of nitric oxide and the plasma concentration of homocysteine (r=-0.592, P<0.0001) and ADMA (r=-0.789, P<0.0001). These significant correlations were found to persist, even when they were restricted to the Alzheimer's patients. The inhibition of endothelial nitric oxide synthesis by ADMA impairs cerebral blood flow, which may contribute to the development of Alzheimer's disease. Endothelial dysfunction is also associated with atherosclerosis and stroke, which are important risk factors for Alzheimer's disease. Inflammation plays an important role in Alzheimer's disease and the inhibition of endothelial nitric oxide by ADMA may increase the concentration of inflammatory mediators in the brain. The inhibition of neuronal nitric oxide synthesis by ADMA may cause cognitive dysfunction in Alzheimer's disease.
...
PMID:Increased concentrations of homocysteine and asymmetric dimethylarginine and decreased concentrations of nitric oxide in the plasma of patients with Alzheimer's disease. 1292 48

Endothelial dysfunction (ECD) is the earliest phenotypic change in the vasculature following exposure to atherothrombotic risk factors. ECD is associated with decreased synthesis and increased oxidative inactivation of nitric oxide (NO). Critical antioxidant enzymes essential for eliminating reactive oxygen species that can inactivate NO include the superoxide dismutases, the glutathione peroxidases, catalase, and glucose-6-phosphate dehydrogenase. Deficiencies of these enzymes increase oxidative stress and NO inactivation and, as such, can either lead to ECD or account for the underlying mechanism of ECD associated with a given atherothrombotic risk factor. Selected antioxidants improve intracellular redox state and reverse ECD by improving the bioavailability of NO. These observations provide mechanistic insights into the molecular basis of ECD in vascular disease and its treatment.
...
PMID:Oxidative stress in endothelial cell dysfunction and thrombosis. 1367 76

The endothelium exerts fundamental control over vascular tone, and injury to the endothelium followed by dysfunction is an early key event preceding manifestation of vessel pathology. Both elevated plasma homocysteine and low folate status have been identified as major and independent risk factors for atherosclerosis and have stirred an enormous and still increasing interest. The damaging effects of hyperhomocysteinemia on endothelial function are, at least in part, reversible through folate supplementation. Because of the inverse relationship between plasma folate and homocysteine levels, however, it is difficult to discriminate between their respective effects. Endothelial dysfunction refers mainly to reduced bioavailability of nitric oxide (NO), which is involved in homocysteinemediated vascular damage. Accumulating evidence further suggests that radical oxygen species are fundamentally involved in hyperhomocysteinemia. NO production is determined by cofactors such as tetrahydrobiopterin, which is oxidized and depleted in conditions of oxidant stress by peroxynitrite. Deficiency of tetrahydrofolate contributes to uncoupling, turning the NO synthase into a superoxide radical-producing enzyme. It appears that progression of vascular disease is likely to determine the multiple interactions between homocysteine, NO, oxygen radicals and folate. Folate has only recently been found to exert direct anti-oxidative effects and contribute to restoration of impaired NO metabolism. Understanding of the complex interactions between homocysteine, radicals, NO and folate offers promising perspectives in the individual treatment of vascular disease. Thus, preventive and therapeutic strategies may require a more distinct approach and better discrimination of target groups for greatest possible efficacy.
...
PMID:Interactions of homocysteine, nitric oxide, folate and radicals in the progressively damaged endothelium. 1465 24

Endothelial dysfunction is a critical factor in the development of vascular disease in patients with diabetes mellitus. Maintenance of the vascular tone and luminal diameter of a blood vessel is dependent on the net balance of vasoconstrictor and vasodilator forces. In both diabetes and obesity, vascular reactivity is abnormal. After ischemia, carbon dioxide challenge, thermal challenge, or exercise, individuals with diabetes do not exhibit the increase in blood flow or vasodilation observed in persons without diabetes. The mechanisms involved in abnormal reactivity may include both the endothelium and vascular smooth muscle. Major vasodilator factors that act on vascular smooth muscle cells are nitric oxide, prostacyclin, and hyperpolarizing factor. The main vasoconstrictors are endothelin, angiotensin II, norepinephrine, serotonin, and thromboxane A(2). In patients with diabetes, there is an increase in vasoconstrictors and a decrease in vasodilators. Thiazolidinediones (TZDs) improve vasodilative responses, which may be of importance in the treatment of vascular disease. The TZDs have anti-inflammatory effects and suppress free fatty acids and reactive oxygen species at the endothelial level, which may contribute to the improved vascular reactivity observed in patients treated with these agents. In addition, these effects of TZDs may have implications for reducing the incidence and severity of atherosclerosis in the long term.
...
PMID:Vascular reactivity and thiazolidinediones. 1467 71

Endothelial dysfunction occurs early in the atherosclerosis in response to elevated atherosclerotic risk factors, and endothelial dysfunction itself may exacerbate the atherosclerotic process. Treatments that reduce atherosclerotic risk factors also generally improve endothelial function. The present review seeks to summarize the effect of exercise training on endothelial function in human subjects. Cross-sectional studies comparing healthy physically active and inactive subjects as well as longitudinal exercise training studies of healthy individuals show little effect of exercise training on endothelial function. In contrast, both cross-section and longitudinal studies document improved endothelial function with exercise training in subjects with abnormal baseline endothelial function, including the elderly and patients with heart failure or coronary artery disease. Improvements in endothelial function with physical activity may explain some of the benefits of exercise in subjects with, or at risk for, vascular disease.
...
PMID:The effect of physical activity on endothelial function in man. 1473 70

Hypothyroidism patients have increased cardiovascular risk, although the mechanism is not defined. Endothelial dysfunction may initiate atherosclerosis, is present in patients with hypothyroidism, and therefore may link hypothyroidism and vascular disease. We are unaware of studies examining the effect of thyroid replacement therapy on endothelial function in hypothyroid patients. The present study examined the effect of treatment of hypothyroidism on brachial artery reactivity. Consequently, we measured endothelium-dependent (EDV) and endothelium-independent (EIV) vasodilation using brachial artery ultrasonography in 8 hypothyroid patients (5 men, mean age 48.9 +/- 5.5 years; mean thyrotropin [TSH] 49.0 +/- 37.0 mIU/L) before and after thyroxine treatment. Thyroxine treatment reduced average TSH to 2.9 +/- 0.5 mIU/L and improved EDV (8.0% +/- 4.4% v 3.4% +/- 2.5%, P <.05), whereas EIV was unchanged (20.3% +/- 6.1% v 19.2% +/- 9.4%, P = not significant [NS]). Thyroxine treatment did not alter serum lipids. Thyroid replacement therapy improves endothelium-dependent vascular reactivity in patients with hypothyroidism irrespective of lipid changes.
...
PMID:Treating hypothyroidism improves endothelial function. 1501 36

Coronary vascular disease is one facet of a generalized disturbance of vascular function present throughout the vascular tree. Dysfunction of the endothelium leads to thickening of the intima and media of the vessel wall of large and medium-sized muscular arteries and large elastic arteries, such as the aorta, carotid, and iliac arteries. Flow-mediated dilatation of the brachial artery is one of several tests used to assess dysfunction of the endothelium using high resolution ultrasound. Endothelial dysfunction has been demonstrated in children with heterozygous familial hypercholesterolemia, type 1 diabetes, morbid obesity, and homozygous homocystinuria and in the offspring of a parent with early coronary disease. High resolution ultrasound has also confirmed postmortem findings that atherogenesis has its beginnings in childhood and adolescence, with the demonstration of increased carotid artery intima-medial thickening in children with familial hypercholesterolemia, familial combined hyperlipidemia, and type 1 diabetes and in the offspring of a parent with early coronary disease. In combination with family history and traditional risk factors, ultrasound evaluation of brachial artery flow-mediated vasodilation and carotid artery intima-medial thickening could be used in a clinical setting to assess coronary risk in high risk pediatric patients.
...
PMID:Clinical review 168: What vascular ultrasound testing has revealed about pediatric atherogenesis, and a potential clinical role for ultrasound in pediatric risk assessment. 1524 May 74

GLP-1 stimulates insulin secretion, suppresses glucagon secretion, delays gastric emptying, and inhibits small bowel motility, all actions contributing to the anti-diabetogenic peptide effect. Endothelial dysfunction is strongly associated with insulin resistance and type 2 diabetes mellitus and may cause the angiopathy typifying this debilitating disease. Therefore, interventions affecting both endothelial dysfunction and insulin resistance may prove useful in improving survival in type 2 diabetes patients. We investigated GLP-1's effect on endothelial function and insulin sensitivity (S(I)) in two groups: 1) 12 type 2 diabetes patients with stable coronary artery disease and 2) 10 healthy subjects with normal endothelial function and S(I). Subjects underwent infusion of recombinant GLP-1 or saline in a random crossover study. Endothelial function was measured by postischemic FMD of brachial artery, using ultrasonography. S(I) [in (10(-4) dl.kg(-1).min(-1))/(muU/ml)] was measured by hyperinsulinemic isoglycemic clamp technique. In type 2 diabetic subjects, GLP-1 infusion significantly increased relative changes in brachial artery diameter from baseline FMD(%) (3.1 +/- 0.6 vs. 6.6 +/- 1.0%, P < 0.05), with no significant effects on S(I) (4.5 +/- 0.8 vs. 5.2 +/- 0.9, P = NS). In healthy subjects, GLP-1 infusion affected neither FMD(%) (11.9 +/- 0.9 vs. 10.3 +/- 1.0%, P = NS) nor S(I) (14.8 +/- 1.8 vs. 11.6 +/- 2.0, P = NS). We conclude that GLP-1 improves endothelial dysfunction but not insulin resistance in type 2 diabetic patients with coronary heart disease. This beneficial vascular effect of GLP-1 adds yet another salutary property of the peptide useful in diabetes treatment.
...
PMID:Effects of glucagon-like peptide-1 on endothelial function in type 2 diabetes patients with stable coronary artery disease. 1535 7


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---