Cardiovascular Actions of Cadmium at Environmental Exposure Levels

Kopp, SJ; Glonek, Thomas; Perry, Horace M.; Erlanger, M; Ef, Perry

doi:10.1126/science.6213041

Cited by 101 publications

(30 citation statements)

References 11 publications

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“…Some workers have observed cardiotoxicity in rats that had about 5 µg/g Cd in their cardiac tissues. 16) Compared to the present study, this concentration is higher than that in the N rats fed Cd and D rats fed Cd. These results indicate that cardiotoxicity may not occur in N rats fed Cd and D rats fed Cd.…”

Section: Resultscontrasting

confidence: 47%

“…A reference flow rate was required for measurement of RBF. Carbonized microspheres (NEN-TRAC, specific activity 9.7 Ci/g), 16 ± 0.1 µm in diameter and labeled with 141 Ce, were suspended in physiological saline with 0.01% Tween 80. The suspension (0.25 ml), containing 80000 microspheres and corresponding to a 0.2-µCi source of radioactivity for 141 Ce, was injected and a reference sample collected from the right femoral artery at a constant rate of 0.41 ml/min with a constant withdrawal Harvard pump (Holliston, MA, United States).…”

Section: )mentioning

confidence: 99%

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Effect of Magnesium Deficiency on Blood Pressure in Normal Rats Fed Cadmium

Nishiyama

Onosaka

Sakai

et al. 2005

JOURNAL OF HEALTH SCIENCE

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We attempted to further define the effects of an Mg-deficient diet on blood pressure in rats fed Cd for long periods. Twenty male Wistar rats were grouped according to four different diets: normal diet (N rats); normal diet supplemented with Cd at a dose of 50 µg/g of diet (N rats fed Cd); Mg-deficient diet (D rats); and Mg-deficient diet supplemented with Cd at a dose of 50 µg/g of diet (D rats fed Cd). Each diet was given for 60 days. N rats fed Cd developed a duration-limited increase in blood pressure: by day 60, increased blood pressure returned to the level seen in N rats. Mg deficiency lowered the Cd-induced increase in blood pressure and this response was more pronounced on day 60. A variety of independent blood pressure regulatory mechanisms was investigated. Although Mg deficiency tended to occur at lower concentrations of Cd and metallothionein in the heart of N rats fed Cd and the Cd concentration was less than 5 µg/g of tissue, Mg deficiency increased the Ca concentration in the hearts of N rats fed Cd while a decrease in urinary Na excretion and an increase in water retention were not observed. Diet-related toxic clinical signs in D rats fed Cd induced marked blush on the ears and fingers, indicating vasodilatation had occurred. These findings may have been a factor in the pronounced reduction in blood pressure seen.

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Section: Resultscontrasting

confidence: 47%

Section: )mentioning

confidence: 99%

Effect of Magnesium Deficiency on Blood Pressure in Normal Rats Fed Cadmium

Nishiyama

Onosaka

Sakai

et al. 2005

JOURNAL OF HEALTH SCIENCE

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“…Enhanced responses to heat, pain, cold stress, and noise were all demonstrated in experimental and human hypertension. 40 In addition, hypertension may be increased by such stressful stimuli as heavy metal 41 and ethanol. 42 The…”

Section: Discussionmentioning

confidence: 99%

Thermosensitivity, a possible new locus involved in genetic hypertension.

et al. 1989

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Spontaneously hypertensive mice have been characterized as more sensitive to environmental heat than normotensive mice. A breeding program was therefore initiated to examine the possible genetic link between thennosensitivity and hypertension. Crossbreeding of spontaneously hypertensive mice with randomly bred normotensive mice produced F, hybrids, which were then intercrossed to create a F 2 population. Thermosensitivity was measured with a noninvasive method. The rate of body temperature increase was significantly (p<0.001) higher in the hypertensive mice (1.74±0.04° C/min) compared with normal controls (1.13±0.03° C/ min). The frequency distribution of the rate of body temperature increase among the progenies was consistent with the hypothesis that a single gene locus determines the observed difference in thermosensitivity between normal and hypertensive mice. The allele that determines the rate of body temperature increase in normal mice was dominant in relation to the allele contributed by hypertensive mice. In the F 2 population, a bimodal distribution determined two phenotypes: less than 1.40° C/min and greater than 1.40° C/min. A significant difference (p<0.0l) in blood pressure of 11 mm Hg was observed between these two phenotypes. In addition, a positive correlation (p<0.01) was noted between the rate of body temperature increase and blood pressure in the F 3 progeny. We conclude that there is possibly a single locus controlling thermosensitivity, which exhibits additive-dominance inheritance. Alleles of this particular trait segregate in part with an increment in blood pressure. The results support the possibility that the increased thermosensitivity seen in hypertensive mice is associated with one of the genes that contributes to their high blood pressure. (Hypertension 1989;14:121-128)

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“…Nutritional modifiers include sodium, 1 calcium, 2 alcohol, 3 excessive caloric intake, 4 and elevated levels of dietary trace elements, such as cadmium. 5 Stressful environmental influences are represented by pain, 6 immobilization stress, 78 and environmental temperature. 9 Hypertensive animals are lethally sensitive to increased environmental temperature, a phenomenon observed in spontaneously hypertensive rats (SHR), 10 -12 as well as in genetically hypertensive mice 13 and hyperthermia-sensitive pigs.…”

mentioning

confidence: 99%

Increased transcription of a major stress gene in spontaneously hypertensive mice.

1990

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Environmental stress factors, including temperature, modify the severity of hypertension, a genetic disease. Hypertensive animals and humans respond abnormally to heat exposure, and this abnormality is reflected at the cellular level by an increment in a major stress (heat-shock) gene expression. The present studies demonstrate that increased hsp70 gene expression is due to its heightened transcription rate. The genetic basis of environmental susceptibility to hypertension may thus involve an abnormal control of heat-shock genes. (Hypertension 1990; 15:904-908)

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Cardiovascular Actions of Cadmium at Environmental Exposure Levels

Cited by 101 publications

References 11 publications

Effect of Magnesium Deficiency on Blood Pressure in Normal Rats Fed Cadmium

Effect of Magnesium Deficiency on Blood Pressure in Normal Rats Fed Cadmium

Thermosensitivity, a possible new locus involved in genetic hypertension.

Increased transcription of a major stress gene in spontaneously hypertensive mice.

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