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At least 19 recordsLinked to original sources
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↗
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↗
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↗
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↗
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↗
PubMed1999

Effects of antioxidants on vascular health.

Substantial in vitro and animal model evidence implicates the free radical-mediated oxidation of low density lipoprotein and its subsequent preferential uptake by macrophages in the arterial intima as an important factor in the development of vascular disease. In addition, antioxidants which prevent the oxidation of LDL in vitro also reduce the severity of vascular disease in animal models. Although some epidemiological studies also suggest that inadequate antioxidant status is related to the development of vascular disease, particularly cardiovascular disease, results from intervention trials have been contradictory. Whereas vitamin E may have a role in reducing the incidence of vascular disease, evidence is less strong for vitamin C, flavonoids and beta-carotene. Additionally, supplementation with some antioxidants such as beta-carotene may increase the incidence of cancer in high risk groups. Although increasing antioxidant intake is generally beneficial for health, this should perhaps be achieved by an increased dietary intake of antioxidant-rich foods rather than by use of supplements.

Animals↗
PubMedDate not supplied

Vascular effects of environmental oestrogens: implications for reproductive and vascular health.

Environmental oestrogens are defined as xenobiotics structurally resembling oestrogen, and are divided into two broad categories, xeno-oestrogens and phyto-oestrogens. Environmental oestrogens may contribute importantly to the increased incidence of reproductive disorders in the modern environment. Although the mechanisms by which environmental oestrogens induce their deleterious effects on the reproductive system remain poorly defined, it is likely that the vascular effects of these compounds play a critical role. In this regard, oestradiol strongly regulates both angiogenesis and vascular remodelling by influencing the growth and function of vascular endothelial cells (EC) and smooth muscle cells (SMC). Since blood vessels, by undergoing angiogenesis, vascular regression and vascular remodelling, actively participate in the normal functioning of reproductive organs, environmental oestrogens-by mimicking or antagonizing the vascular effects of oestradiol-may induce abnormalities in vascular function and structure leading to reproductive disorders such as pre-eclampsia, endometriosis, impaired follicular development, inefficient implantation, impotence and infertility. The purpose of the present review is to summarize the evidence regarding the vascular effects of xeno-oestrogens and phyto-oestrogens and to discuss the implications for these effects on the reproductive system.

Animals↗
PubMed1991

Evaluating quality, cost-effective health care. Vascular database predicated on hospital discharge abstracts.

This population-based study examines all carotid endarterectomies (CE) performed by all surgeons in a single state over a 10-year period. The methodology is designed to determine morbidity rate, mortality rate, cost, and length of stay, as well as to understand the effect of pre-existing chronic disease, physician, and hospital volume on these outcome variables. The data source consisted of hospital discharge abstract data uniformly collected on all admissions (N = 5.9 million) to acute care hospitals in the state. In the decade 1979 to 1988, 11,199 patients underwent CE. Mortality rate from CE was 2.1%, and the postoperative stroke rate was 3.7% over this period. High physician volume decreased the mortality rate (p less than 0.05) and stroke rate (p less than 0.01) by 50% and significantly (p less than 0.001) reduced hospital cost and length of stay independent of patient complexity. Examination of cost data, adjusted for inflation, showed a decrease in mean cost for CE over the decade. Thus physicians are providing better care for less hospital dollars. Both patient and payor outcome is improved by concentrating CE patients in the hands of high-volume surgeons. Although the data suggests this trend is already evolving, the pace of this evolution can be expected to increase as payors recognize that regionalization of this procedure lowers costs.

Arteriosclerosis↗
PubMed1977

Blood and vein-wall fibrinolytic activity in health and vascular disease.

The resting blood fibrinolytic activity of 120 normal subjects and 294 patients with various forms of vascular disease was assessed by measuring the dilute blood clot lysis time and fibrin plate lysis area before and after 10 minutes of venous congestion. The tissue fibrinolytic activity of several of these subjects was assessed in vein biopsy specimens. The results suggested that there was a correlation between blood and tissue fibrinolytic activity and that certain venous diseases, particularly recurrent superficial thrombophlebitis and venous liposclerosis, were associated with a deficiency of blood and tissue fibrinolytic activity.

Fibrinolysis↗
PubMed1995

17 beta-estradiol stimulates prostacyclin, but not endothelin-1, production in human vascular endothelial cells.

The exact mechanisms by which estrogens protect against occlusive vascular disorders are not known. One possibility could be an effect on vascular endothelial vasoactive compounds, such as vasodilatory prostacyclin (PGI2) and vasoconstrictory endothelin (ET-1). Here we report on the effect of 17 beta-estradiol on the synthesis of PGI2 and ET-1 in cultured human umbilical vein endothelial cells. These cells were incubated in the absence (control) and presence of 17 beta-estradiol (0.001-1 mumol/L) for 3-24 h with serum (10%) or without serum. The release of PGI2, as assessed by its metabolite 6-keto-prostaglandin F1 alpha, and that of ET-1, were assessed by RIA. 17 beta-Estradiol (0.01-0.1 mumol/L) predissolved in ethanol (final concentration, 0.01%) increased PGI2 production by 26-30% in endothelial cells incubated without serum. This increase in PGI2 production was enhanced up to 66% when 17 beta-estradiol (1 mumol/L) was encapsulated within beta-cyclodextrin. The stimulation of PGI2 production was detectable after 12 h of incubation. The 17 beta-estradiol-induced stimulation of PGI2 production was blocked in dose-dependent manner by antiestrogenic tamoxifen. 17 beta-Estradiol failed to affect the production of PGI2 if the endothelial cells were incubated with serum and had no effect on ET-1 production under any conditions. 17 beta-Estradiol-induced stimulation of vasodilatory and antiaggregatory PGI2 production without a concomitant change in vasoconstrictory ET-1 production may provide one explanation for the ability of estradiol to maintain vascular health and protect against vascular disorders.

6-Ketoprostaglandin F1 alpha↗