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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The frequencies of 10 diseases in a cadmium (and zinc) contaminated region in The Netherlands were analysed by comparing hospital admissions with those of a non-contaminated region and with national values. No significant differences were found for diseases which are commonly associated with increased cadmium uptake such as renal insufficiency, nephrolithiasis, hypertension, cancer, immaturity of the new-born. For the contaminated region a significantly higher frequency was only found for atherosclerosis; this was relatively strong for men aged > 40 yrs. However, no higher death frequency for atherosclerosis was observed. The results are discussed in relation to limitations in the evaluation techniques used. The absence of major health risks in the contaminated area is obvious, but the possible influence of long term-low level cadmium uptake on atherosclerosis requires more attention.
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PMID:Prolonged low-level cadmium intake and atherosclerosis. 825 93

Cadmium, a trace element from natural and industrial sources, may contribute to the pathogenesis of arterial hypertension. We evaluated the effect induced by acute intracerebroventricular (icv) administration of cadmium on mean blood pressure of normotensive conscious rats. Intracerebroventricular cadmium (1 to 10 micrograms) produced a dose-dependent, sustained increase in mean blood pressure. The hypertensive response to icv cadmium was significantly (P < .01) prevented by icv pretreatment with verapamil (10 to 100 micrograms). A preventive effect was exerted also by icv nifedipine (100 micrograms); however, this result was attributable, at least in part, to the antihypertensive action of the vehicle, polyethylene glycol. The hypertensive response to icv cadmium was blunted by icv administration of 10 ng clonidine, 10 micrograms vasopressin antagonist, or 10 micrograms bradykinin antagonist (P < .05), but it was not altered by icv enalaprilat (100 micrograms). These results indicate that brain calcium channels play a role in the hypertensive action induced by icv cadmium. Accumulation of cadmium in the brain caused by prolonged exposure to this heavy metal might lead to chronic arterial hypertension.
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PMID:Verapamil prevents the acute hypertensive response to intracerebroventricular cadmium in conscious normotensive rats. 846 5

Cadmium, an environmental pollutant, is known to induce hypertension in animal models, in part via an increase in peripheral vascular resistance. Since prior studies have investigated the vascular effects of cadmium using large, nonresistance arteries, we directly assessed cadmium's action on resistance size arterioles in skeletal muscle using the intact rat cremaster muscle preparation. Cadmium evoked a concentration-dependent constriction of the large arterioles (120 to 50 microns in diameter) but elicited no change in the diameter of smaller arterioles (30 to 15 microns). Blockade of alpha-adrenergic receptors did not diminish the constrictor response of the larger arterioles to cadmium, but bathing the cremaster muscles with a solution containing low calcium attenuated the arteriolar constriction to cadmium. Calcium repletion caused the arterioles to constrict further. These observations provide the first direct evidence that cadmium constricts resistance arterioles in skeletal muscle. The cadmium constriction: (1) is selective for the large arterioles, (2) is not mediated by alpha-adrenergic receptors, and (3) is influenced by the extracellular level of calcium. We conclude that arteriolar constriction in skeletal muscle tissue may play a role in the hypertensive actions of cadmium.
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PMID:Cadmium-induced arteriolar constriction in skeletal muscle microcirculation. 850 53

The Cadmibel Study is a cross-sectional population study, which investigated the hypothesis that environmental exposure of the population to cadmium would result in health effects. The 2,327 participants constituted a random sample of the population of four Belgian districts, chosen to provide a wide range of environmental exposure to cadmium. The urinary cadmium excretion, a measure of lifetime exposure, averaged 9.3 nmol/24h in men (range 0.4-325 nmol/24h) and 7.2 nmol (0.1-71 nmol/24h) in women. The Cadmibel Study refuted the hypothesis that exposure to cadmium would lead to an increase in BP and in the prevalence of hypertension and other cardiovascular diseases. Serum alkaline phosphatase activity and the urinary excretion of calcium correlated significantly and positively with urinary cadmium in both sexes. These findings suggest that the calcium metabolism is gradually affected, as cadmium accumulates in the body. Furthermore, several markers of renal tubular function (urinary excretion of retinol binding protein, N-acetyl-beta-glucosaminidase, beta 2-microglobulin and aminoacids) were significantly and positively associated with urinary cadmium. There was a 10% probability of abnormal values of these markers of tubular function when urinary cadmium exceeded +/- 20 nmol/24h. However, the morbidity associated with the functional changes, observed in the Cadmibel Study, remains presently unknown and requires further investigation, preferably in a longitudinal population studies.
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PMID:Health effects of environmental exposure to cadmium in a population study. 851 95

To investigate the chronic low-level environmental cadmium and zinc exposure of Chinese women and find the relationships between these parameters and hypertension, 58 women without histories of smoking and occupational exposure were conducted into this cross-section study and divided into three groups: Group I: 24 normal healthy, Group II: 24 untreated essential hypertension, and Group III: 10 untreated nonessential hypertension women. The serum cadmium and daily urinary cadmium excretion of Group II (1.69 +/- 0.92 micrograms/L; 2.43 +/- 1.93 micrograms/d) were significantly higher than those of Group I (0.88 +/- 0.92 micrograms/L; 1.07 +/- 1.45 micrograms/d) as well as Group III (0.92 +/- 0.91 micrograms/L; 0.19 +/- 0.23 micrograms/d). The ratio of urinary zinc (micrograms)/urinary creatinine (g) of Group II (865.99 +/- 460.54 micrograms/g) was higher than that of Group I (622.39 +/- 250.96 micrograms/g). The ratio of urinary cadmium concentrations (micrograms)/urinary creatinine (g) of all healthy Chinese women was 1.30 +/- 1.67 which is higher than that of other nations in the world except Japanese. After adjusting age and body mass index, we found mean arterial pressure positively correlated with serum cadmium in all subjects (p = 0.0058). The mean arterial pressure also positively correlated with serum cadmium (p = 0.0017) as well as daily urinary cadmium excretion (p = 0.0088) in all women except the nonessential group. Both the ratios of urinary zinc (micrograms)/urinary creatinine (g) (p = 0.0165) and urinary cadmium (micrograms)/urinary creatinine (g) positively (p = 0.0246) related to mean arterial pressure in women of Group I and II.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased body cadmium burden in Chinese women without smoking and occupational exposure. 852 85

This article presents recent data on several environmental toxins: lead, carbon disulfide, asbestos, arsenic, ozone, cadmium, vinyl chloride, fluorocarbons, freon, and pesticides. These environmental toxins produce both hypertension and cardiac arrhythmias in most studies, and they are not necessarily related to primary lung disease and secondary heart disease. The possible mechanisms that could cause the cardiovascular diseases include (1) damage to the endothelial barrier in the vascular system, (2) activation of leukocytes and platelets, (3) initiation of plaque formation, (4) stimulation of the inflammatory response, (5) kidney-related hypertension, and (6) direct damage to cardiac and blood vessel tissue. Recommendations are that more animal, human cultured cell, and epidemiologic studies should be conducted on the environmental toxins identified in this article.
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PMID:Cardiovascular effects of environmental chemicals. 863 34

In order to investigate the role of increased lipid peroxidation in the development of cadmium-induced hypertension, 30 male albino rats were exposed to drinking water containing 15 micrograms/ml cadmium for 30 days, and the results were compared with those of 30 controls. Water containing high cadmium concentrations caused a significant accumulation of the element in blood and kidneys, associated with an obvious elevation in blood pressure. The systolic and diastolic blood pressures rose from 102.8 +/- 7.0 and 81.2 +/- 3.8 mm Hg to 128.1 +/- 4.6 and 107.9 +/- 7.4 mm Hg, respectively, in cadmium-treated rats (p < 0.01). A decreased glomerular filtration rate and increased serum creatinine levels were accompanied by elevated levels of cortical and medullary thiobarbituric acid reactive substances in cadmium-induced hypertensive rats. The mean thiobarbituric acid reactive substance level rose from a control value of 211.5 +/- 64.1 to 303.3 +/- 46.3 nmol/g protein (p < 0.01) in the renal cortex due to the high intake of cadmium. Despite its obvious diuretic and natriuretic action in control animals, the bolus injection of 1.2 and 2.4 micrograms/kg atrial natriuretic peptide corrected neither elevated blood pressure nor the reduced glomerular filtration rate in rats exposed to cadmium. However, the tubular response to atrial natriuretic peptide remained unaltered. These data suggest that a lack of vascular response to atrial natriuretic peptide is one of the many putative causes of cadmium-induced hypertension, and cadmium-mediated increased lipid peroxidation may be involved in this unresponsiveness.
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PMID:Role of cadmium-induced lipid peroxidation in the kidney response to atrial natriuretic hormone. 868 36

Two train conductors had chest tightness, painful breathing, muscle cramps, and nausea after fighting a fire in a battery box under a passenger coach. Shortly thereafter, they became anosmic and had excessive fatigue, persistent headaches, sleep disturbances, irritability, unstable moods, and hypertension. Urinary cadmium and nickel levels were elevated. Neurobehavioral testing showed, in comparison to referents, prolonged reaction times, abnormal balance, prolonged blink reflex latency, severely constricted visual fields, and decreased vibration sense. Test scores showed that immediate verbal and visual recall were normal but delayed recall was reduced. Scores on overlearned information were normal. Tests measuring dexterity, coordination, decision making, and peripheral sensation and discrimination revealed abnormalities. Repeat testing 6 and 12 months after exposure showed persistent abnormalities. Cadmium and vinyl chloride are the most plausible causes of the neurotoxicity, but fumes from the fire may have contained other neurotoxic chemicals.
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PMID:Persistent neurotoxicity from a battery fire: is cadmium the culprit? 868 56

The relation between trace elements and human health has been scarcely studied. With respect to cardiovascular diseases and hypertension attention has mostly focused on arsenic, cobalt, copper, chromium, fluorine, manganese, vanadium, zinc, selenium, silicon, cadmium, and lead. Environmental contamination can influence organ concentrations through long-term, low-level effects. This article reviews the present knowledge obtained by epidemiological, biochemical and cell biological studies. Attention is paid to interpretation problems due to the complexity of biochemical interactions with proteins of various sorts which determine metabolic processes and to the occurrence of detoxification mechanisms in which trace elements interact. This can also lead to strong variations in individual vulnerability. In general, the elements selenium, copper, zinc, chromium, and manganese seem to counteract the development of cardiovascular diseases, whereas cadmium and may be lead seem to stimulate it. Effects of arsenic, silicon and fluorine are unclear and for cobalt absent. The intensity of these effects on public health is difficult to measure, but is as yet probably limited except in extra-ordinary situations.
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PMID:Trace elements and cardiovascular diseases. 878 27

The CadmiBel Study was a cross-sectional population study that investigated the health effects of environmental exposure to cadmium and lead. The 2327 participants constituted a random sample of the population of four Belgian districts, chosen in order to provide a wide range of environmental exposure to cadmium. After adjustment for confounding factors, such as smoking and occupational exposure, the urinary cadmium excretion, a measure of lifetime exposure, was nearly 30% higher in the polluted areas. The CadmiBel Study produced evidence inconsistent with the hypothesis that environmental exposure to cadmium and lead would lead to an increase in blood pressure and to a higher prevalence of hypertension and other cardiovascular diseases. On the other hand, the serum alkaline phosphatase activity and the urinary excretion of calcium were significantly and positively correlated with urinary cadmium in both sexes. These findings suggested that the homeostasis of calcium was gradually affected as cadmium accumulated in the body. Furthermore, several markers of renal tubular dysfunction (urinary excretion of retinol-binding-protein, N-acetyl-beta-glucosaminidase, beta 2-microglobulin and amino acids) were significantly and positively associated with urinary cadmium. Across 10 small areas of which six were polluted with cadmium, an inverse association existed between the creatinine clearance and several indexes of environmental exposure to cadmium (cadmium concentration in the soil, cadmium content of locally grown vegetables, the inhabitants' 24 h urinary cadmium excretion). In the CadmiBel Study, the creatinine clearance was also inversely correlated with the concentrations of lead and zinc protoporphyrin in the blood. Thus, environmental exposure to cadmium and lead was associated with alterations in renal function. The significance in terms of morbidity and mortality of the functional disturbances observed in the CadmiBel Study, and the possible strategies to prevent the transfer of cadmium from the environment to man are under investigation in the prospective PheeCad Study in which half of the Cadmibel participants have been enrolled (participation rate 80%).
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PMID:Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Working Groups. 878 28


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