Role of Cadmium in Human and Experimental Hypertension

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Abstract
Acute and chronic studies performed in our laboratory in normal rabbits, dogs, human control subjects, and patients with hypertension are reviewed. Cadmium, a common contaminant of air, water, and food, produces persistent hypertension in the rabbit and dog. The pervasive metal is predominantly deposited in the kidney and liver, and to a lesser extent in the blood vessels of the cadmium-hypertensive rabbits. Vascular responsiveness to angiotensin in the cadmium-hypertensive aortic strips was significantly lower than that of the strips obtained from control normotensive rabbits. Cadmium-hypertensive aortic strips also developed significantly lower passive tension on step-wise increase in the original length of the strips (strain). Administration of cadmium acetate directly into the renal artery, preceding the injection of the vasopressor (angiotensin, epinephrine or norepinephrine), resulted in a dose-related reversible inhibition of the vasopres-sor-induced renal vasoconstriction. It is probable that significant pathophysi-ological changes in experimental cadmium hypertension would occur in the vascular system and the kidney, where cadmium deposition was the greatest. Mean plasma cadmium levels were significantly higher in patients with hypertension. Plasma zinc levels, however, were significantly lower only in hypertensive patients wilh renovascular and renal parenchymal disease but not in essential hypertension patients. A program of detailed epidemiological studies and public health measures is needed for further definition of the role of cadmium in “idiopathic” human hypertension.

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