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

Social, economic, and medical variables correlated with "psychogenic" death rates across about 30 countries. However, McClelland's psychological motives of achievement, affiliation, and power, determined for each country by content analysis of children's stories, did not. Status integration correlated positively with homicide and negatively with deaths from suicide and ulcers. Low life expectancy, wealth, economic growth, wine consumption, and zinc (cadmium) consumption correlated with deaths from homicide, suicide, ulcers, cirrhosis and hypertension, respectively.
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PMID:"Psychogenic" death: a reappraisal. 546 Jun 5

Cadmium (Cd) produces injurious effects on reproductive function and has been implicated in the pathogeneses of hypertension. The present article summarizes available data on alterations in the cyclic AMP system of testicular and prostatic tissue as well as in catecholamine metabolism in adrenal glands following exposure to Cd and subsequent withdrawal. Daily Cd (1 mg/kg IP) for 45 days decreased prostatic and testicular weights of mature male rats. In prostate, chronic treatment with Cd reduced cyclic AMP levels to 57% of normal values which appeared to be due to the decrease in adenylate cyclase activity since cyclic AMP metabolism by phosphodiesterase was not significantly altered. Cyclic AMP binding to prostatic protein kinase was increased following Cd administration as was the activity of the cyclic AMP-dependent form of protein kinase. In contrast to the prostate, testicular adenylate cyclase was stimulated by Cd treatment. However, the endogenous cyclic AMP levels remained unaffected since the increase in testicular adenylate cyclase was offset by a concomitant increase in the activity of phosphodiesterase. Although the activities of the cyclic AMP-dependent and the independent forms of testicular protein kinase were significantly depressed, the binding of cyclic AMP to protein kinase from testes of Cd-treated rats was not affected. Discontinuation of treatment for 28 days in rats that had previously been given the heavy metal for 45 days resulted in at least a partial reversal of several of the cadmium-induced changes in cyclic AMP metabolism of the rat prostate and testes. However, the weight of the prostate glands remained essentially in the same range as that seen in the "treated group."Data suggest that cyclic AMP metabolism in both the primary and the secondary reproductive organs is altered following chronic Cd treatment and that some changes persist even 28 days following the termination of daily exposure to the heavy metal.Cd treatment also increased adrenal weights and augmented the levels of adrenal norepinephrine and epinephrine as well as the activity of tyrosine hydroxylase. Discontinuation of the heavy metal treatment for 28 days, in rats previously injected with Cd 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 withdrawal of Cd 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 Cd toxicity might be related to increased synthesis of epinephrine in adrenal glands.
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PMID:Testicular cyclic nucleotide and adrenal catecholamine metabolism following chronic exposure to cadmium. 611 36

Changes in sympathetic nervous function of the rat caused by acute and chronic treatment with cadmium ((Cd2+) have been studied in vivo by measurement of changes in blood pressure and plasma dopamine-beta-hydroxylase (DBH) activity. In anaesthetized animals, acute injection of Cd2+ (0.1-1 microM) caused an initial fall followed by a rise in both diastolic and systolic blood pressure, plasma DBH activity increased in a dose-dependent manner. Animals subjected to repeated treatment with Cd2+ (0.5, 1 microM) daily for 12 days became markedly hypertensive, the increases in the systolic pressure being greater than those seen in the diastolic pressure. In pithed animals the blood pressure responses of the treated animals to electrical stimulation of the lower sympathetic outflow (T10-L1) and tyramine injection (35, 70, 140 nmol kg-1) were markedly decreased, whilst responses to low doses of noradrenaline (NA) (7, 15, 30 nmol kg-1) were potentiated compared with untreated animals. In addition, plasma DBH activities following sympathetic outflow stimulation and tyramine administration were markedly increased and decreased respectively compared with untreated controls. The data suggest that a correlation exists between changes in sympathetic nervous function and the induction of hypertension caused by Cd2+.
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PMID:The effects of cadmium ions on blood pressure, dopamine-beta-hydroxylase activity and on the responsiveness of in vivo preparations to sympathetic nerve stimulation, noradrenaline and tyramine. 611 20

The present study focuses on the interaction between cadmium (Cd) and the Na, K-ATPase system in in vitro grown vascular smooth muscle cells (VSMCs) derived from the rat carotid artery. In disrupted VSMCs rendered permeable by osmotic shock, Cd inhibited Na, K-ATPase; I50 was reached at 10(-5) M Cd. Mg-ATPase was also inhibited by Cd; I50 was attained at concentrations of 10(-4) M Cd. Cd inhibition of Na,K-ATPase in the VSMCs was noncompetitive with respect to Na, K, and ATP. Rubidium transport experiments performed with intact VSMCs demonstrated that within an incubation period of 150 minutes, a concentration of 10(-4) M Cd in the extracellular fluid exerted no acute effect on the Na-K pump. Within this time interval, intracellular Cd attained a concentration eightfold higher than the extracellular Cd concentration. Thus, it appears that under acute conditions Cd exerts its inhibitory effect on Na, K-ATPase only in disrupted VSMCs. The data further suggest that, in the VSMC, conditions under which Cd inhibits Na, K-ATPase are consistent with inhibition from the cytoplasmic side of the cell membrane.
Hypertension
PMID:Cadmium effect on the Na,K-ATPase system in cultured vascular smooth muscle cells. 614 Nov 42

In 1962 Schroeder reported marked hypertension in rats chronically fed a very low cadmium diet and 5 ppm cadmium in water, but subsequently he reported only moderate hypertension. Using Schroeder's food and water, but a slightly less cadmium-free environment, we repeatedly induced mild hypertension with 5 ppm cadmium, mild because control pressures were higher not because cadmium-fed animals had lower pressures. Seven laboratories have observed hypertension after feeding cadmium; six have not. Thus, chronically fed cadmium can induce hypertension in rats, but conditions are important. Additional observations on cadmium-induced hypertension indicate that: (1) concentrations from 0.1 to 5 ppm cadmium in water are pressor; (2) sex, strain, and age of animals are apparently not limiting factors; (3) there is associated sodium retention; (4) there is a concomitant decrease in the high energy phosphate content of tissues. Rats with cadmium-induced hypertension have renal cadmium concentrations which bracket those of the average environmentally exposed American or European. Finally, renal cadmium concentrations in man were significantly higher (p less than 0.05) for "hypertensives" than for normotensive "matches" in five of nine reported series, lower in one, and similar in three, with all series being small and suboptimal in subject selection.
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PMID:Does cadmium contribute to human hypertension. 634 13

The health effects of human exposure to cadmium are discussed with emphasis on intake, absorption, body burden, and excretion; osteomalacia in Japan; hypertension; and proteinuria, emphysema, osteomalacia, and cancer in workers. Elevated blood pressure has not been observed as a result of excessive exposures to cadmium in Japan or the workplace. Renal tubular dysfunction and consequent proteinuria is generally accepted as the main effect following long-term, low-level exposure to cadmium. Studies of workers show that proteinuria may develop after the first year of exposure or many years after the last exposure. Proteinuria and deterioration of renal function may continue even after cessation of exposure. The immediate health significance of low-level proteinuria is still under debate. However, there is evidence that long-term renal tubular dysfunction may lead to abnormalities of calcium metabolism and osteomalacia. The few autopsy and cross-sectional studies of workers do not permit conclusions to be drawn regarding the relationship between cadmium exposure and emphysema. Retrospective and historical-prospective studies are needed to settle this important question. No conclusive evidence has been published regarding cadmium-induced cancer in humans. However, there is sufficient evidence to regard cadmium as a suspect renal and prostate carcinogen. Because of equivocal results and the absence of dose-response relationships, the studies reviewed should be used with caution in making regulatory decisions and low-dose risk assessments.
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PMID:Human health effects of exposure to cadmium. 636 79

Cadmium has been shown to manifest its toxicity in human and animals by mainly accumulating in almost all of the organs and kidney is the main target organ where it is concentrated mainly in cortex. Environmental exposure of cadmium occurs via food, occupational industries, terrestrial and aquatic ecosystem. At molecular level, cadmium interferes with the utilization of essential metals e.g. Ca, Zn, Se, Cr and Fe and deficiencies of these essential metals including protein and vitamins, exaggerate cadmium toxicity, due to its increased absorption through the gut and greater retention in different organs as metallothionein (Cd-Mt). Cadmium transport, across the intestinal and renal brush border membrane vesicles, is carrier mediated and it competes with zinc and calcium. It has been postulated that cadmium shares the same transport system. Cadmium inhibits protein synthesis, carbohydrate metabolism and drug metabolizing enzymes in liver of animals. Chronic environmental exposure of cadmium produces hypertension in experimental animals. Functional changes accompanying cadmium nephropathy include low molecular weight proteinuria which is of tubular origin associated with excess excretion of proteins such as beta 2 microglobulin, metallothionein and high molecular weight proteinuria of glomerular origin (excretion of proteins such as albumin IgG, transferrin etc.). Recent data has shown that metallothionein is more nephrotoxic to animals. Cadmium is also toxic to central nervous system. It causes an alterations of cellular functions in lungs. Cadmium affects both humoral and cell mediated immune response in animals. Cadmium induces metallothionein in liver and kidney but under certain nutritional deficiencies like protein-calorie malnutrition and calcium deficiency, enhanced induction and greater accumulation of cadmium metallothionein has been observed.
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PMID:Molecular basis of cadmium toxicity. 638 35

Many studies showed the unhealthy effect of smoking on the fetus. Several mechanisms for the unfavorable effect are discussed. In the last few years interest has been shown in the occurrence of heavy metals such as cadmium and lead in smoke. In animal experiments high doses of cadmium showed mutations, teratogenicity and low doses showed retardation of fetal growth. Amniotic fluid examinations of smoking and non-smoking pregnant women showed that there is no barrier to cadmium from the placenta. A direct correlation between cigarette smoking and cadmium concentration in the amniotic fluid was found. Cadmium was discussed as a reason for hypertension. But this was not verified in our study. There were no correlations between the cadmium and lead content of amniotic fluid and the gestational age, and disturbances of the pregnancy nor a correlation to the incidence of abortions. The lead concentration in the amniotic fluid of smokers and non-smokers showed no significant difference. This is attributed to the ubiquitous exposition to lead with increasing pollution of the environment. The relatively small additional amounts of lead in cigarettes do not increase the amount of lead in the amniotic fluid.
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PMID:[Cadmium and lead concentrations in the amniotic fluid of pregnant smokers and non-smokers]. 655 81

A comparative study of renal cadmium burdens in a group of thirty hypertensive patients undergoing treatment and in a group of thirty matched controls is reported, both groups being volunteers selected from a non-occupationally exposed population. The aim of this study was to investigate the possible involvement of cadmium in the aetiology of hypertension at the chronic low levels of environmental exposure. Renal cadmium levels were measured in vivo, using the technique of partial-body neutron activation analysis. The results showed that the mean renal cadmium level in the hypertensive group [3.3 mg (SD 2.3)], was not significantly different from that [4.4 mg (SD 2.7)], in the normotensive group. Whether the level in the hypertensives depends on the treatment is open to question and will be the subject of further investigation. In addition, the results confirm that kidney cadmium levels are elevated in smokers.
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PMID:An in-vivo study of renal cadmium and hypertension. 678 63

Essential trace elements such as zinc, iron, and copper participate in various enzyme reactions directly related to the regulation of blood pressure and indirectly related to generation of oxidative metabolic energy, alterations in blood lipid levels, and alterations in taste acuity. The toxicological action of several heavy metal ions including cadmium, lead, mercury, and thallium can cause hypertension by affecting hormone metabolism, vasoconstriction, and renal tubular function. We conclude, however, that neither deficiencies of essential elements nor the presence of toxic heavy metals are primary causes of hypertension in our population.
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PMID:Trace elements and blood pressure. 684 20


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