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Because high barium concentrations (2-10 ppm) in human drinking water have been reported to be associated with elevated cardiovascular mortality, hypertension and other cardiovascular effects were sought in rats chronically exposed for 1-16 mo to drinking water containing 1, 10, or 100 ppm barium. From weaning, female Long-Evans rats were kept in a "low contamination" environment and fed a diet low in trace metals. Their drinking water was deionized, fortified with 5 essential trace metals, and either 0, 1, 10, or 100 ppm barium was added. Indirect systolic pressure of unanesthetized rats was measured in triplicate at 1, 2, 4, 8, 12, and 16 mo. Average systolic pressure increased significantly after exposure to 100 ppm barium for 1 mo or longer and after exposure to 10 ppm barium for 8 mo or longer. After 4 or 16 mo, barium exposure failed to alter organ weights or tissue concentrations of calcium, magnesium, sodium, or potassium; however, both 10 and 100 ppm barium resulted in significant increases in tissue barium. Rats exposed to 100 ppm Ba for 16 mo exhibited depressed rates of cardiac contraction and depressed electrical excitability in the heart. Hearts from these maximally exposed rats also had significantly lower ATP content and phosphorylation potential, as measured by 31P NMR spectroscopy. Although the barium-induced increase in the blood pressure of rats was modest, comparable mild hypertension in humans would have major health implications.

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The aim of this experiment was to test whether a chelating agent, D-myo-inositol-1,2,6-trisphosphate (PP56), could reverse cadmium-induced hypertension. Four groups of weanling female Long-Evans rats received ad libitum a rye-based, metal-poor diet and deionized water fortified with essential metals for 15 mo from the time of weaning. A control group received neither cadmium nor chelating agent. A second group had 0.1 ppm cadmium added to their water from weaning through mo 5. A third group had 60 ppm PP56 added to their water for mo 6-10. The fourth group had 0.1 ppm cadmium added to their water from weaning through mo 5 and 60 ppm PP56 from mo 6-10. All groups were followed without either cadmium or PP56 for mo 11-15. At approximately monthly intervals, systolic pressure was measured by the indirect tail cuff method in unanesthetized rats. Chronic cadmium feeding induced the expected hypertension, with an average increase in systolic pressure of about 15 mm Hg; the pressor effect persisted with little change for the 10 mo after cadmium was withdrawn. PP56 completely reversed the cadmium-induced hypertension, and the inhibition persisted for 5 mo after PP56 was withdrawn. PP56 by itself had no demonstrable depressor effect.

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Groups of 15 to 18 female weanling Long-Evans rats fed a rye-based diet low in lead (0.25 ppm) were exposed to 0.1, 1.0, and 5.0 ppm lead in drinking water. No suggestion of clinical lead toxicity was recognized. Systolic pressures were measured at 3-month intervals after weaning. The groups of lead-exposed animals had consistently and significantly higher average pressures than control animals, the increase approximating 15 mm Hg. With the lowest lead exposure (0.1 ppm), the increase in average pressure was gradual, being half minimal at 3 months and requiring 1 year to become maximal. After 1 year, half of these rats had pressures from 0 to 10 mm Hg above the control average; 40, 20, and 10% had pressures that were 20, 30, and 40 mm Hg, respectively, above the control average. Thus, rats exposed to lead in amounts comparable to the environmental exposure of many Americans had an average elevation in systolic pressure comparable to that of human beings with essential hypertension.

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One percent salt, 1 ppm cadmium, or 1 ppm cadmium plus 1 ppm lead in drinking water caused similar mild hypertension in rats. The hypertensive effect of salt, given for 4 months beginning at weaning, disappeared when the salt was withdrawn but subsequently returned without further exposure. Rats continuously given 1 ppm cadmium during and after salt exposure were continuously hypertensive, but salt did not increase their hypertension. Rats continuously exposed to cadmium or cadmium plus lead without extra salt remained hypertensive for 20 months. Rats exposed to cadmium or cadmium plus lead for months 4 through 8 remained hypertensive after metal exposure was discontinued; addition of 0.35 ppm selenium corrected the hypertension in cadmium-fed rats but had little effect in the cadmium plus lead exposed rats.

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Long-term exposure to cadmium in drinking water can induce hypertension in rats. We have consistently observed that from 0.1 to 5 ppm cadmium in deionized drinking water fortified with five essential metals induces a significant pressor effect in female Long-Evans rats on a noncommercial, low cadmium, rye-based diet. To test the effect of diet, a commercial stock diet (Purina Rodent Lab Chow), with either fortified or plain deionized water, was begun at weaning in rats that were receiving water containing 0.1 or 1 ppm cadmium. The overall effect of substituting the stock diet for the rye diet was initially to lessen, and later to prevent entirely, the cadmium-induced pressor effect. Whereas control rats on the rye diet have a constant systolic pressure of about 100 mm Hg throughout the experiment; control rats on the stock diet had an increase in systolic pressure of about 1 mm Hg/month, perhaps because of cadmium from food which contained 10 times as much of the metal as the rye diet. (There was also a somewhat lower pressure among the cadmium-fed rats on stock diet than among those on the rye diet). There were other (non-cadmium) differences between the stock and rye diets and between the remainder of our experimental conditions and those used by other investigators, presumably explaining the failure of some others to induce hypertension with cadmium.

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Chronic feeding of non-toxic doses of cadmium induces an average increase of 15 to 20 mm Hg in indirectly measured systolic pressure of lightly anaesthetized rats. The mechanism of this increase is not known, but cadmium has several potentially pressor effects, including increased sodium retention. This report describes both sodium balance and blood pressure in a pair of experiments where cadmium was fed and in a pair where it was injected. All four cadmium challenges induced sodium retention and also induced hypertension. Thus, rats with either low or moderate chronic exposure to fed cadmium (well below the exposures required to induce toxicity) retained more intraperitoneally injected radiosodium than controls and at the same time developed higher systolic pressures than controls. Immediately following intraperitoneally injected cadmium, rats lost a radiosodium more rapidly than controls; in both situations the blood pressure was higher than the controls. These data indicate that some of the pressor effect associated with cadmium exposure could result from its concomitant antinatriuretic effect.

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In a low cadmium environment, adding 10 parts per million (ppm) of cadmium to the drinking water of rats for 3 to 18 months induced increases in systolic pressure averaging 12 to 18 mm Hg. The pressor effect of the cadmium was inhibited by adding 3.6 ppm of selenium or 200 ppm of zinc to the drinking water or by dissolving the cadmium in hard water rather than deionized water. A second experiment with 2.5 ppm of cadmium and smaller amounts of selenium and zinc was confirmatory. Exposure to 10 ppm of cadmium increased renal, hepatic, and cardiac cadmium many fold from barely detectable control levels; however, the increases were much less when the cadmium was dissolved in hard water. Cadmium exposure also increased tissue zinc by 30 to 60%. The addition of selenium to cadmium further increased cardiac cadmium, but the addition of zinc to cadmium had no further effect on tissue cadmium. Tissue selenium concentrations were suggestively but not significantly higher following selenium exposure. Cadmium alone, or combined with selenium or zinc, increased renal copper; while the combination of cadmium and selenium increased hepatic copper.

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