Cadmium: hypertension induction and lead mobilization.
In recent years interest has increased in the study of the metabolism of cadmium because of its presence in the environment as a toxic agent. Having no known essential bodily functions and possibly altering the action of various other trace metals, eg, lead and zinc, cadmium has been suspect as a causative factor in certain pathological alterations, such as hypertension. A study of this association was undertaken by the authors.Female Sprague-Dawley rats were fed laboratory chow and given cadmium nitrate ad libitum. Systolic pressure was monitored and weights were recorded at weekly intervals. Cadmium and lead were determined in kidney and liver tissues of the sacrificed animals by using a trace metal analyzer and by atomic absorption spectrophotometer. After 36 weeks on the experimental regimen, the cadmium-treated animals had higher systolic pressures than the control group (155 ± 10 mmHg compared to 96 ± 5 mmHg). Increased levels of cadmium reflective of the cadmium consumed were found to occur in liver and kidney tissues. The urinary excretion of deltaaminolevulenic acid by the experimental animals was higher than that of the control animals. This suggests that the supplemented cadmium induced lead to leave the kidney and become metabolically active.
D000818:Animals; D002104:Cadmium / Q000008:administration & dosage / Q000009:adverse effects* / Q000378:metabolism; D005260:Female; D006973:Hypertension / Q000139:chemically induced* / Q000378:metabolism; D007668:Kidney / Q000378:metabolism; D007854:Lead / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D051381:Rats
D002104:Cadmium; D007854:Lead