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At least 19 recordsLinked to original sources
PubMed2004

Arginine and endothelial and vascular health.

The vascular endothelium is a crucial regulator of vascular function and homeostasis. Nitric oxide (NO) is an important paracrine substance released by the endothelium to regulate vasomotor tone. Risk factors for atherosclerosis, as well as atherosclerosis per se, are associated with endothelial dysfunction and decreased bioavailablilty of NO. Indeed, endothelial dysfunction is integral to the pathogenesis of atherosclerosis and other cardiovascular diseases. Moreover, endothelial dysfunction relates to an increased risk of adverse cardiovascular outcomes. L-Arginine is an essential amino acid required by the constitutive enzyme, endothelial NO oxide synthase (eNOS), to produce NO. Administration of L-arginine improves endothelial function in animal models and in humans with hypercholesterolemia and with atherosclerosis. Clinical trials to date support potential clinical applications of L-arginine in the treatment of coronary artery disease and peripheral arterial disease, as well as in the prevention of in-stent restenosis. The mechanism of benefit of L-arginine on endothelial function is unclear, because intracellular concentrations of L-arginine far exceed that required by eNOS. One potential explanation of this "arginine paradox" is that L-arginine restores endothelial function in atherosclerotic patients, in whom there are elevated levels of asymmetric dimethylarginine, an endogenous inhibitor of eNOS. Given the promising findings of early studies of L-arginine as a potential therapy for cardiovascular disorders, large-scale clinical trials are warranted.

Animals↗
PubMedDate not supplied

Amino acids, arginase and nitric oxide in vascular health.

1. Nitric oxide (NO) plays a fundamental role in the vasculature because of its diverse influence in vascular protection, including its well-reported antiproliferative, anti-inflammatory, antithrombotic and vasodilator effects. In many vascular disease states, NO production is reduced as a result of endothelial dysfunction, in part caused by a decrease in substrate (L-arginine) availability. 2. The role of L-arginine and other amino acids important in nitrogen balance has been re-examined in the context of their effects on vascular health. The metabolism of L-arginine is complex because it is involved in a plethora of other pathways, such as urea, creatine and agmatine production. L-Arginine supplementation in patients with vascular disease is well reported to benefit patients therapeutically because of its effect on both NO-dependent and -independent mechanisms. 3. L-Arginine availability depends on the flux of other amino acids in the body, including L-glutamine, L-glutamate, L-ornithine, L-citrulline and L-lysine. The role of L-methionine and homocystine and their effect on NO also play an influential role in the body. 4. Recent data suggest that the key enzyme involved in the L-arginine-urea cycle, arginase, is coexpressed in NO-producing cells in the vasculature. In the present review, we examine the potential role of arginase as a therapeutic target for vascular health.

Amino Acids↗
PubMedDate not supplied

The role of the renin-angiotensin system in vascular health: use of ACE inhibition to improve vascular function.

Hypertension is a syndrome in which dysfunction of the blood vessels and of neuroendocrine systems play a major role. Arteriosclerosis and atherosclerosis are distinct processes in arterial disease. Arteriosclerosis begins with thickening and hardening of the arterial wall, with loss of elasticity. Atherosclerosis is an inflammatory process that begins with endothelial dysfunction, and leads to vascular occlusion. The endothelial dysfunction that causes atherosclerosis and coronary artery disease results from an imbalance between nitric oxide and angiotensin-II. This balance becomes tipped toward angiotensin-II in the presence of hypertension. When arteries stiffen as a result of hypertension and aging, they are not able to store blood volume properly, systolic blood pressure rises, and pulse pressure widens. Because the tissue renin-angiotensin system is responsible for promoting the adverse structural arterial changes, inhibition of angiotensin-converting enzyme (ACE) is effective in restoring the health of both large and small arteries by blocking angiotensin and by increasing bradykinin.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2007

Acute effects of periodontal therapy on bio-markers of vascular health.

AIM: We aimed to study the impact of periodontal therapy on several bio-markers related to vascular health. MATERIAL AND METHODS: Fifty-five consecutive subjects (age range 30-64 years) having severe periodontitis received an intensive session of periodontal therapy under local anaesthesia and provided blood samples before and 1 and 7 and 30 days following therapy. High-sensitivity assays were utilized to quantify serum concentrations of inflammatory markers [interleukin (IL)-1beta, tumour necrosis factor-alpha], plasma haemostatic (D-dimer) and endothelial soluble markers [soluble E-selectin (s-Es) and von Willebrand factor antigen (r-WF:Ag)]. RESULTS: Periodontal therapy elicited a significant activation of the haemostatic system (38% and 68% mean increases of plasma D-dimer 1 and 7 days after therapy, respectively, p<0.001), together with moderate endothelial dysfunction (10% and 30% mean increases at 24 h in plasma soluble E-selectin, p<0.05 and von-Willebrand factor, p<0.01, respectively). D-Dimer and s-Es acute changes were significantly correlated with periodontal treatment time (p<0.05). Cigarette smoking status and body mass index strongly influenced the acute release of IL-1beta (p<0.05), D-dimer (p<0.01) and s-Es (p<0.01). CONCLUSIONS: Periodontal therapy represents a novel and reliable non-drug-induced model to investigate in vivo the interplay between inflammation, coagulation and endothelial cell activation.

Acute-Phase Reaction↗
PubMed1985

Favourable levels of cardio-vascular health and risk indicators during childhood and adolescence.

This paper is concerned with favourable levels of constitutional cardio-vascular health indicators during childhood and adolescence. A cross-sectional randomised sample of healthy Czechoslovakian children was investigated, because this population is habituated to a favourable life style. Twenty girls and 20 boys at ages 8, 12 and 16 years were recruited to the study. Statistical data for means and standard deviations are presented with regard to maximal aerobic power, haemodynamic variables such as arterial blood pressure, heart rate at submaximal and maximal muscular exercise, body fat content, blood lipids including total cholesterol and its fractions, high- and low-density lipo-proteins, fasting triglycerides and the apo-lipo-protein profile. The maximal oxygen uptake in absolute values increased with age in both sexes and the boys appeared to average higher than the girls at each age. When maximal aerobic power was expressed on a total body weight basis, boys appeared to average higher at age 16 years (56 ml X min-1 X kg-1) than girls (45.8 ml X min-1 X kg-1). The highest recorded heart rate for ergometric work averaged close to 200 min-1 in both sexes with no significant age differences. The diastolic blood pressure at rest did not change significantly with age or sex. Serum cholesterol levels were found to decrease significantly after puberty in boys (post-pubertal dip), but in the girls there was found no systematic change in mean values with age. When HDL was expressed as a percentage of total cholesterol there appeared to be no differences related to age and sex.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2001

Angiotensin-converting enzyme inhibition to enhance vascular health--clinical and research models.

Protection of the endothelium, the metabolically active inner lining of the vasculature, appears to be a key factor in maintaining cardiovascular (CV) health. The endothelium responds to hemodynamic and hormonal factors by secreting substances that maintain vascular homeostasis. Damage to the endothelium is an initial step in the development of CV disease. Angiotensin-converting enzyme (ACE) inhibitors, which block the formation of the vasoconstricting substance, angiotensin II, have proved to be a key therapy for hypertension and congestive heart failure. The activity of these agents in enhancing vascular health appears to be a critical factor in their therapeutic effectiveness. Large-scale clinical trials over the past decade have shown that ACE inhibition is an effective therapeutic means of not only prolonging survival and reducing morbidity after acute myocardial infarction, but also reducing all-cause mortality and morbidity in patients at high risk for CV disease, including patients with diabetes. ACE is found in far greater amounts in tissue than in plasma. Studies indicate that ACE inhibitors act at the tissue level to provide long-term cardioprotective effects that include a reduction in the progression of atherosclerosis. An issue to resolve is how much ACE inhibition is needed at the tissue level to reverse or prevent further vascular damage.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2004

Beyond deficiency: potential benefits of increased intakes of vitamin K for bone and vascular health.

Vitamin K is well known for its role in the synthesis of a number of blood coagulation factors. During recent years vitamin K-dependent proteins were discovered to be of vital importance for bone and vascular health. Recommendations for dietary vitamin K intake have been made on the basis of the hepatic requirements for the synthesis of blood coagulation factors. Accumulating evidence suggests that the requirements for other functions than blood coagulation may be higher. This paper is the result of a closed workshop (Paris, November 2002) in which a number of European vitamin K experts reviewed the available data and formulated their standpoint with respect to recommended dietary vitamin K intake and the use of vitamin K-containing supplements.

Antifibrinolytic Agents↗
PubMed1999

Oxidants downstream from superoxide inhibit nitric oxide production by vascular endothelium--a key role for selenium-dependent enzymes in vascular health.

Although superoxide can directly quench endothelium-generated nitric oxide (NO), there is considerable evidence that oxidants derived from superoxide--notably peroxides and their further derivatives--can also impair NO bioactivity. In part, this reflects inhibition of NO synthase activity, perhaps mediated by the oxidation of labile sulfhydryl groups, as well as the activation of protein kinase C. Selenium deficiency exacerbates these effects, presumably owing to the crucial role of selenium-dependent thioredoxin reductase and glutathione peroxidases in preventing and reversing oxidant damage to proteins. High-normal homocyst(e)ine levels may induce an 'effective selenium deficiency' by suppressing glutathione peroxidase transcription in endothelial cells. Considerable epidemiology, primarily of European origin, points to mediocre selenium nutrition as a significant vascular risk factor; the risk associated with elevated plasma homocyst(e)ine levels is now well established. In addition to preventing LDL oxidation, vitamin E can be expected to minimize the contribution of lipid peroxides to endothelial dysfunction. Lipoic acid, which can function in vivo as a versatile antioxidant and sulfhydryl reductant, may have particular value for protecting endothelium from oxidants; its clinical utility in diabetic neuropathy may reflect this benefit. Good selenium status, as well as supra-nutritional intakes of lipoic acid, may down-regulate cytokine-mediated endothelial activation by helping to maintain the proper structure of oxidant-labile proteins--such as tyrosine phosphatases--that modulate this signaling. It can be concluded that a number of supplemental nutrients--including selenium, vitamin E, lipoic acid, and the vitamins that promote catabolism of homocysteine--have the potential to promote vascular health by mitigating the adverse impact of superoxide-derived oxidants on endothelial function.

Cytokines↗
PubMed2002

Vascular health risks in the Aboriginal community. A cultural approach.

BACKGROUND: Diabetes, heart disease and other vascular diseases are a great problem in Aboriginal communities and there are many reasons for this. As a health professional it is easy to feel overwhelmed by both the magnitude of the problem and the feeling that it is just too hard when patients don't seem to take charge of their own health. OBJECTIVE: This article aims to outline the increased vascular disease and vascular risk factors in the Aboriginal community and explore some of the historical, socio-economic, cultural and genetic reasons for this. The barriers to health care and self management are discussed and some positive developments in the area of Aboriginal vascular health are noted. DISCUSSION: To improve health outcomes we need to focus on two parts of the same problem. First, we need to tackle the vascular diseases at their roots--the vascular risk factors. Second, we need to look at ways to promote self management so that our patients can identify personal barriers to self care and be partners in their health care. There is evidence that better organised systems of care, such as recall systems and improved screening systems, are very beneficial. The most successful interventions are culturally appropriate and developed and implemented with Aboriginal community control.

Attitude to Health↗
PubMed2006

Monitoring vascular health beyond blood pressure.

It is well recognized that vascular changes, including atherosclerosis, begin early in life as a silent, asymptomatic disease process and are associated with cardiovascular (CV) risk factors. Importantly, CV risk factors persist or track from childhood to adulthood and are predictive of CV disease risk in adults. Evaluation of arterial stiffness and its predictors may help identify asymptomatic individuals at risk, before blood pressure is elevated above an "arbitrary" level that we currently identify as hypertension. Currently, measurements of arterial stiffness are being used in the research setting and also as part of cardiovascular risk prediction clinics. As the various techniques become more widely available, it is conceivable that the measurement of arterial stiffness could become an important part of the routine assessment of patients in daily practice, as a supplement to blood pressure measurement. Measurement of arterial stiffness will not only be helpful in the detection of early vascular disease but also will be a tool in the follow-up monitoring of strategies aimed at preventing hypertension or reducing further progression of vascular disease before blood pressure elevation can be detected.

Atherosclerosis↗
PubMed1999

Endothelial membrane potential regulates production of both nitric oxide and superoxide--a fundamental determinant of vascular health.

There is recent evidence that the membrane potential of vascular endothelium regulates not only nitric oxide (NO) synthesis, but also superoxide generation, such that hyperpolarization stimulates NO production while suppressing that of superoxide. Given that NO works in a variety of ways to inhibit atherothrombotic disease and hypertension, whereas superoxide not only vetoes the benefits of NO but also disrupts endothelial metabolism and promotes LDL oxidation through its oxidant activity, it is thus evident that endothelium membrane potential is a crucial determinant of cardiovascular risk. Membrane polarization can be enhanced by measures which increase the synthesis or availability of the Na+-K+-ATPase, moderately enhance serum K+ and increase the conductance of membrane K+ channels. Such measures may include high-K+/low-Na+ natural diets, insulin sensitizing modalities, 'euthyroid replacement therapy' and ACE inhibitors. Epidemiological correlations of insulin resistance with hypertension and cardiovascular risk may reflect the low membrane potential of insulin-resistant vascular endothelium. Adjunctive measures for suppressing the generation or half-life of endothelial superoxide are suggested.

Aldosterone↗
PubMed2006

Treating vascular risk factors and maintaining vascular health: is this the way towards successful cognitive ageing and preventing cognitive decline?

Dementia is a progressive disorder that typically worsens with time and from which recovery is unlikely. The incidence of dementia increases exponentially with ageing and is an important public health challenge. There is now growing evidence for the role of vascular factors in Alzheimer's disease, mixed dementia (Alzheimer's disease with cerebrovascular disease), and of course vascular dementia. With the rising prevalence of vascular disease, there are increasing numbers of people who are identified to be at risk of cognitive impairment. By changing modifiable vascular risk factors, there is emerging evidence that it may be possible to prevent or delay the expression and progression of dementia.

Aged↗
PubMed2004

The pivotal role of nitric oxide for vascular health.

The endothelium is a single cell layer that lines all blood vessels. This tissue produces an impressive array of paracrine factors that maintain vascular homeostasis. One of these factors is the potent vasodilator endothelium-derived nitric oxide (NO). Impairment in the synthesis or bioactivity of NO, as manifested by reduced endothelium-dependent vasodilation, has been shown to be an independent risk factor for major adverse cardiovascular events. The linkage between endothelium-derived NO and cardiovascular health is likely due to the pleiotropic effects of NO on the vessel wall. NO inhibits the proliferation of vascular smooth muscle cells, the aggregation of platelets, and the adherence and infiltration of inflammatory cells. Thus, an impairment of NO bioactivity or synthesis will reduce its braking effect on processes involved in atherogenesis. New insights have been made regarding the mechanisms by which NO bioactivity becomes impaired. Cardiovascular risk factors induce vascular oxidative stress, which accelerates the degradation of NO. In addition, oxidative stress causes the accumulation of asymmetric dimethylarginine (ADMA). ADMA is an endogenous inhibitor of NO synthesis. Elevation of ADMA appears to be a common mediator by which cardiovascular risk factors impair NO synthesis. Elevation of plasma ADMA has been linked to impaired endothelium-dependent vasodilation, carotid intimal thickening and adverse cardiovascular events. A number of modern therapies directed against atherosclerosis also improve the function of the NO synthase pathway. New agents that specifically target the NO synthase pathway have been developed, and represent a new front on the war against heart disease.

Arginine↗
PubMed2001

Predicting the future of vascular health care: the impact of the baby boom generation.

With the aging of the "Baby Boomers," the need for vascular care will be substantial. Three things predominate: (1) variability in distribution of the work force, (2) increasing use of all vascular procedures, and (3) marked geographic variation as to who receives vascular therapy. The mandate to standardize therapy with the least resource utilization and the best results will only strengthen with time.

Aortic Aneurysm, Abdominal↗
PubMed2006

The effect of iron status on vascular health.

The effect of increased iron stores on the progression of atherosclerosis and endothelial health remains inconclusive. This study was designed to evaluate the relationship between hemochromatosis genotypes, serum ferritin levels and presymptomatic vascular abnormalities in a cohort of healthy subjects. Carotid intima-media thickness (CIMT) and brachial flow-mediated vasodilation (FMD) were assessed by high-resolution ultrasound in 907 male (47 +/- 10 years) participants enrolled in the Firefighters and their Endothelium (FATE) study. Analyses of the hemochromatosis C282Y, H63D and S65C alleles were simultaneously determined by a single nucleotide polymorphism (SNP) primer extension method. It was found that brachial FMD was not related to serum ferritin or hemochromatosis genotype status. The presence of a hemochromatosis-associated genotype (n = 18) or heterozygosity for the C282Y genotype (n = 98) was not associated with an increased mean CIMT. After adjustment for conventional risk factors, serum ferritin was also not associated with mean CIMT. In conclusion, neither ferritin nor a hemochromatosis genotype was related to brachial endothelial function or carotid atherosclerosis. The present study does not support the hypothesis that mild to moderately increased iron stores are associated with enhanced atherosclerosis risk.

Adult↗
PubMed2006

Moderate resistance training and vascular health in overweight women.

PURPOSE: Impaired endothelial function has been implicated as an initial step in the pathogenesis of atherosclerosis leading to cardiovascular disease (CVD). Aerobic exercise improves vascular function and reduces risk of CVD morbidity and mortality; however, the effects of resistance training on vascular function remains unclear. Thus, the aim of this study was to examine the effects of 1 yr of resistance training (RT) on vascular structure and function in overweight but otherwise healthy eumenorrheic women. METHODS: Study participants consisted of 30 (15 control, 15 RT) overweight (BMI > 25 kg x m(-2)) women, aged 24-44 yr, studied before and after a 1-yr RT intervention. Vascular structure and function were assessed via noninvasive ultrasound imaging of the carotid and brachial arteries, respectively. Body composition, blood pressure, and fasting blood lipids and glucose also were measured. RESULTS: The RT group demonstrated a significant mean improvement in one-repetition maximum bench press following 1 yr of RT (P < 0.05). There also was a significant increase in lean body mass in the RT group compared with the control group (P = 0.04). There were no training-associated changes in blood pressure, fasting blood lipids, glucose, or insulin levels. Although there was no change in carotid artery intimamedia thickness, peak flow-mediated dilation significantly improved in the RT group (P < 0.05). CONCLUSION: The principal significant finding in this study was the initial demonstration that RT alone can improve brachial artery endothelial function in overweight eumenorrheic women.

Adult↗