Control rats and rats with experimental renal hypertension due to unilateral stenosis of one renal artery received a standard diet (0.23% sodium) and a sodium-deficient diet (0.004% sodium), alternately, during which time blood pressure and plasma renin activity were determined. At the end of the experiment, renin content of the kidneys was measured. In normotensive control rats, the sodium-deficient diet did not affect blood pressure, but plasma renin activity and renin content of the kidneys increased. In rats with renal hypertension, restriction of sodium supply was followed by a fall in blood pressure to normotensive levels, provided that an intact contralateral kidney was present. Similarly, sodium-deficient diet prevented the development of hypertension if given immediately after placing the clip on one renal artery. Restriction of sodium supply provoked a marked increase in plasma renin activity, whereas renin content of the ischemic kidney was only slightly, but significantly, higher than in rats with normal sodium intake. Contrary to this, in unilaterally nephrectomized rats with renal hypertension, neither hypertension nor plasma renin activity or renin content of the kidneys was affected by sodium-deficient diet. In control rats with unilateral nephrectomy, plasma renin activity was only half that of intact rats, and restriction of sodium provoked no more than an increase up to normal values of intact rats. Sodium loss by the contralateral kidney may contribute to both the antihypertensive effect of a sodium-deficient diet and the increase in plasma renin activity.

1.In renal hypertensive rats, increase in blood pressure above 180 mmHg may induce sodium and water loss, reduced growth rate, elevated haematocrit, a marked rise in plasma renin concentration, an increase in renin extractable from the clamped and the contralateral kidney and malignant nephrosclerosis of the contralateral kidney. These symptoms characterize the malignant phase of renal hypertension in rats.2. When water was given as drinking fluid, ten of eighteen rats developed signs of malignant hypertension and malignant nephrosclerosis within 3 4 weeks. Administration of 0.9% saline instead of water induced higher blood-pressure levels, but only five of eighteen rats showed malignant nephrosclerosis. When drinking fluid was changed from water to saline shortly before or shortly after the onset of malignant hypertension, the condition improved, and in only one of twelve rats was malignant nephrosclerosis observed.3. It is concluded that in renal hypertensive rats sodium supplements may improve or prevent signs of malignant hypertension and the development of malignant nephrosclerosis.

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The reaction between hog renin and rat angiotensinogen followed Michaelis-Menten kinetics. A K m value of 1,109 ng angiotensin/ml was determined for the rate of angiotensin formation at pH 7.4 and 37°C. The pH optimum for the reaction of hog renin with rat angiotensinogen was between 6.8 and 7.0. Pepstatin inhibited the reaction in a noncompetitive way. The maximum inhibitory effect occurred at approximately pH 6; at values above pH 8.0, pepstatin had no inhibitory effect. The effect of pepstatin was reversible, since renin activity could be restored by 24 hours of dialysis against distilled water. A 50% inhibition of the enzymatic activity of 0.01 dog units of hog renin was obtained with 0.45 µg pepstatin/ml.