IN A previous communication (1) from this laboratory it was shown that adequate potassium intake is requisite for the development and persistence of hypertension following administration of desoxycorticosterone acetate (DCA) to intact rats. This study suggested the importance of determining the interrelationship of sodium and potassium ions in DCAinduced hypertension and whether or not excessive potassium intake potentiated the pressor effect of DCA. In order to clarify these problems, the present investigation was undertaken. In approximately one half of a series of rats subjected by us to uninephrectomy and the application of a figure-of-eight ligature to the remaining kidney, hypertension failed to develop postoperatively. It was found previously (2) that the administration of DCA rapidly elevated the blood pressures of such normotensive postoperative rats. This method was utilized in the present study to induce hypertension. A series of five-week-old male rats (Long-Evans) was uninephrectomized and a renal ligature applied to the remaining kidney (3). Blood pressures were obtained at weekly intervals postoperatively with the microphonic manometer (4). By the ninth week 48 rats that failed to show systolic blood pressures exceeding 135 mm. of Hg were divided into five groups which thereafter were maintained upon synthetic diets containing varied amounts of sodium and potassium as indicated in the table on page 662. The basic potassium-deficient diet fed to Groups III and V has been described previously (5). During the subsequent ten-week interval all rats received tri-weekly subcutaneous injections of 4 mg. of DCA (in benzyl alcohol) and their blood pressures were determined at weekly intervals.
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Rosenman et al. (1954) studied this question.
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