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1. Pregnancy enhances the susceptibility of the rat to intercurrent renal damage produced by anti-placenta serum. This is manifested by the development of renal hypertrophy and nephritis in a number of these animals. Both renal hypertrophy and nephritis are consistently intensified by the concomitant administration of DCA. 2. Hypertension develops in both pregnant and non-pregnant rats treated with the anti-placenta serum employed together with the daily administration of DCA. 3. Termination of pregnancy, in the face of continued DCA administration, fails to lower the blood pressure or to arrest the nephritic process.

1. Marked hypertension was induced in adrenalectomized rats on a sodium-restricted intake by the administration of cortisone acetate; on a similar regimen, adrenalectomized rats receiving DCA failed to become hypertensive. 2. The incorporation of a liberal amount of sodium in the diet of adrenalectomized rats receiving cortisone acetate resulted in a lesser degree of hypertension; whereas on a similar regimen, DCA-injected animals became strikingly hypertensive, as has been previously reported. 3. The presence of hypertension in the cortisone acetate-treated rats was not associated with histological evidence of renal damage or serum electrolyte disturbance, such as was observed in hypertensive animals receiving DCA. 4. The hypertension in sodium-restricted normal rats receiving cortisone acetate was less striking than in similarly treated adrenalectomized animals. On a liberal sodium intake similar degrees of hypertension were noted in both intact and adrenalectomized groups. 5. To approximate the loss of weight which occurred in cortisone acetate-injected rats, it was necessary to curtail the food intake of partially fasted control groups to 50 to 75 per cent of the amount consumed by the animals receiving the steroid. 6. The serum cholesterol levels of the cortisone acetate-injected rats were consistently and strikingly elevated as contrasted with normal, partially fasted, or DCA-treated animals.

1. The injection of rabbit anti-rat-placenta serums in young adult rats produced chronic glomerulonephritis in 18 of 32 animals. 2. The course of the nephritis and the renal lesions were indistinguishable from those obtained in 11 of 13 animals injected with rabbit anti-rat-kidney serum. 3. Six instances of similar renal lesions occurred among 99 control animals. In 2 the rats had been injected with rabbit anti-rat-erythrocyte serum, in 2 with rabbit anti-rat-serum serum, while in 2 others the lesions were found among normal stock.

1. Desoxycorticosterone acetate (DCA) and NaCl, in the dosage employed in normal rats, caused renal and cardiac hypertrophy, characteristic changes in the renal tubular epithelium, atrophic changes in the subcapsular zone of the adrenal cortex, and serum electrolyte changes characterized by a rise in sodium and fall in potassium. 2. In rats rendered nephritic with a rabbit anti-rat-kidney serum, the same regimen caused similar changes. In addition, DCA given concurrently with NaCl greatly intensified the nephritic process and gave rise to striking arterial hypertension. 3. A diet, virtually sodium-free, administered to normal and nephritic rats receiving daily injections of DCA abolished or reduced to a minimum the effects of this steroid; i.e., a liberal ingestion of NaCl was essential for the potentiation of the action of DCA. 4. The addition of KCl to the drinking water of rats receiving DCA and NaCl tended to correct the depression of the level of potassium in the serum, but had no effect upon the hypertension in nephritic animals nor upon the anatomical lesions. 5. The mechanism by which the sodium ion potentiates the activity of DCA has not been established.