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

Cardiovascular disease is a major cause of morbidity and mortality in the U.K. and other developed countries. In the U.K., mortality from coronary heart disease has increased progressively over the past 25 years, particularly in males. This paper examines the possible role of trace metals in the development of cardiovascular disease, with particular reference to the effects of cobalt, cadmium and lead in myocardial disease, atherosclerosis and hypertension. It is concluded that cobalt is an unimportant factor in community levels of cardiovascular disease, that cadmium has striking effects on blood pressure in animals and that there is some evidence for an association between environmental lead and high blood pressure.
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PMID:Cardiovascular disease and trace metals. 4 Feb 34

Many reports indicate a significant negative correlation between death-rates for coronary heart-disease (C.H.D.) and water hardness. A reverse situation exists in the twin Kansas cities, U.S.A. Kansas City, Kansas, has water which is more than twice as hard as the softened water of Kansas City, Missouri, from the same source. Serum cholesterol and triglyceride levels were similar, but blood-pressure was higher in Kansas City, Kansas, and this correlated with higher serum-sodium, lower serum-potassium, and a tenfold higher serum-cadmium. Serum calcium and magnesium levels were higher in Kansas, while copper, chromium, cobalt, and zinc were higher in Missouri. The serum studies were con ducted on two matched groups of 260 adults from each of the sample cities. Hypertension may account for the reverse C.H.D. rate noted and be cadmium related.
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PMID:Possible toxic water factor in coronary heart-disease. 4 75

Administration of cadmium to laboratory animals causes hypertension. Necropsy specimens of the liver and kidneys of human patients who had had hypertension were previously reported as showing elevated cadmium concentrations. In the present study living normal humans were found to have a blood-cadmium level of 3-4 +/- 0-5 ng/ml, while a matched group of living untreated hypertensive humans had a blood-cadmium of 11-1 +/- 1-5 ng/ml. All of the normal subjects had blood-cadmium levels below 8-0 ng/ml, while 13 of the 17 hypertensive patients had blood-cadmium levels over 8-0 ng/ml.
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PMID:Blood-cadmium levels in normotensive and untreated hypertensive humans. 5 34

70 hypertensive patients and 70 controls matched for age and sex were investigated for a possible relationship between blood-cadmium and hypertension. No significant differences between the two groups were detected, although the blood-cadmium level was significantly higher in smokers as compared to non-smokers. These data do not support the hypothesis that cadmium is involved in the development of hypertension in man.
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PMID:Blood-cadmium in hypertensives and normotensives. 6 43

22 of 31 residents of a Somerset village where soil levels of cadmium were high had raised blood-cadmium levels, and some had clinical and biochemical findings (including hypertension and biochemical evidence of renal tubular damage) indicating toxic effects which could be attributed to the metal. It is suggested that more detailed studies should be carried out as a matter of urgency and that advice on avoiding local garden produce and not smoking should be emphasised. Probably more serious, however, is the summation effect with industrial exposure.
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PMID:Evidence of cadmium toxicity in a population living in a zinc-mining area. Pilot survey of Shipham residents. 8 93

Dahl hypertension-resistant (R) and hypertension-sensitive (S) rats were used to determine whether cadmium-induced hypertension is dependent on genetic predisposition. In experiment I, 16 wk-old R and S rats of both sexes were injected with two doses of cadmium (1 and 2 mg/kg body wt, ip), whereas the controls received the same volumes of saline. Hypertension and renal vascular changes were observed in cadmium-injected S rats but not in R rats. The S females appeared more sensitive than S males to the hypertensinogenic effect of cadmium. In experiment II, groups of weanling female R and S rats were given 0, 1, 2.5, 5, or 10 mg cadmium/liter drinking water and fed either a low-salt (0.4% NaCl) or a high-salt (4% NaCl) diet for 28 wk. Cadmium produced cardiac hypertrophy (1 mg cadmium/liter) and hypertension associated with renal vascular changes (1--5 mg cadmium/ liter), and it enhanced proteinuria (1-10 mg cadmium/liter) in S rats on a low-salt diet. Also, the development of salt-induced hypertension was accelerated in cadmium-fed (1 and 2.5 mg/liter) S rats. These adverse effects of cadmium were not detected in R rats on either salt diet. In experiments I and II, cadmium concentrations in the kidneys and liver of S rats were higher (P less than 0.001) than in those of R rats. These data indicate that genetic differences influence the pathogenesis of cadmium-induced hypertension.
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PMID:Genetic influence on cadmium-induced hypertension. 15 9

Daily intraperitoneal injection of cadmium chloride (1 mg/kg) for 45 days significantly increased adrenal weights and augmented the levels of adrenal norepinephrine and epinephrine as well as the activity of adrenal tyrosine hydroxylase. Discontinuation of the heavy metal treatment for 28 days, in rats previously injected with cadmium for 45 days, restored the activity of tyrosine hydroxylase as well as the amount of norepinephrine and epinephrine. In contrast, adrenal weights were restored only partially following the withdrawal of cadmium treatment. Evidence indicates that the changes in adrenal catecholamine metabolism may be the result of stress induced by chronic exposure to this heavy metal. In addition, some of the untoward effects such as hyperglycemia and arterial hypertension seen during cadmium toxicity might be related to increased synthesis of epinephrine in adrenal glands.
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PMID:Effect of chronic cadmium treatment on rat adrenal catecholamines. 23 28

The suggestion that cadmium-induced hypertension in rats might be due to renal sodium retention, known to result from Cd treatment, was examined. Young female rats were given a regimen of intraperitoneal cadmium treatments reported to cause hypertension reliably within a month. They were sensitized to the development of salt hypertension by removal of one kidney and then given 1 percent saline solution to drink. Over a five-week period, experimental animals consistently drank more saline than controls, despite which fewer of them became hypertensive, with the result that the average systolic pressure of controls finally reached the hypertensive range, whereas the experimental group remained normotensive. Cadmium treatment had no detectable effect on growth, the hemogram, serum Na and K, or the weight of liver, kidney, heart, spleen, thymus, or adrenal glands. There was thus no evidence that cadmium caused any adverse constitutional or hemodynamic effects, but it appeared to retard the development of salt hypertension. The results do not support the suggestion that the hypertensive effects of cadmium are modulated by sodium-retaining influences on the kidney.
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PMID:Effect of cadmium on salt hypertension in rats. 42 35

Surveys of Aleuts on St. Paul Island, Alaska, in 1966 and 1976 found a prevalence of hypertension as high as any reported in the United States. The rate remained high over the 10-year period. Preliminary data from other Aleut villages on the Aleutian Chain indicate that a high prevalence of hypertension may be widespread in this region. Etiologically genetic factors, obesity, and a high salt intake are all present. In addition, an exceedingly high level of cadmium content was found in seal livers, a dietary staple. Isolated locations such as St. Paul provide natural laboratories for possibly elucidating the complex etiology of this disease.
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PMID:Hypertension among Aleuts. 46 66

Exposure of rats to cadmium causes a marked depletion of iron in liver and kidney. Selenium neither counteracts or intensifies the influence of cadmium on tissue iron levels. Selenium injections protect against cadmium-induced testicular damage but cause this element to accumulate in the testes at higher concentration than in animals exposed to cadmium without selenium. Selenium injection diverts the binding of cadmium from low molecular weight proteins to high molecular weight ones. Dosing rats with selenium and cadmium or inclusion of Se or Cd in the diet did not result in altered cadmium binding in tissues, raising some questions concerning the environmental significance of these injection experiments. Addition of selenium to a diet containing cadmium decreased the accumulation of cadmium in liver and kidney, but increased its deposition in testes. The metabolism of cadmium bound to metallothionein was markedly different as compared to the inorganic salt of this element. Dietary ascorbate, but not citrate or cysteine, decreased the deposition of cadmium in rat tissues. In some low-level exposure experiments with cadmium (1 to 1000 ppb), no differences were found in the percentage of dose absorbed or rate of cadmium accumulation when provided in food versus water. Female rats tended to absorb more cadmium than males. The binding of cadmium to cytosolic proteins was found to be different between rats fed low levels of cadmium (up to 1 ppm) as compared to those fed high levels of this element (100 ppm). Cadmium was not found to contribute to hypertension in rats, and a summary of results by various investigators is presented. Blood and hair cadmium levels in Oregon residents were found to be highest in employees of a mine, and hair cadmium was found to be respectively higher in smokers than nonsmokers and in metal workers than office workers. No relationships were observed in humans between blood or hair cadmium levels and blood pressure.
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PMID:Cadmium effects in rats on tissue iron, selenium, and blood pressure; blood and hair cadmium in some oregon residents. 48 28


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