The suggestion that cadmium-induced hypertension in rats might be due to renal sodium retention, known to result from Cd treatment, was examined. Young female rats were given a regimen of intraperitoneal cadmium treatments reported to cause hypertension reliably within a month. They were sensitized to the development of salt hypertension by removal of one kidney and then given 1 percent saline solution to drink. Over a five-week period, experimental animals consistently drank more saline than controls, despite which fewer of them became hypertensive, with the result that the average systolic pressure of controls finally reached the hypertensive range, whereas the experimental group remained normotensive. Cadmium treatment had no detectable effect on growth, the hemogram, serum Na and K, or the weight of liver, kidney, heart, spleen, thymus, or adrenal glands. There was thus no evidence that cadmium caused any adverse constitutional or hemodynamic effects, but it appeared to retard the development of salt hypertension. The results do not support the suggestion that the hypertensive effects of cadmium are modulated by sodium-retaining influences on the kidney.