Depletion of carcass potassium in rats made hypertensive with desoxycorticosterone acetate (DCA) and with cortisone.

The hypertension which can be induced experimentally in rats by the administration of desoxycorticosterone acetate (DCA) differs from that which develops in rats given cortisone acetate in its dependence upon a liberal sodium intake (1). Not only is DCA-hypertension made more severe by providing the animals with excess sodium (2), but it fails to develop if the available supply of this cation be sufficiently restricted (3). In contradistinction, the capacity of cortisone (1) or of hydrocortisone (4) to elevate the blood pressure is independent of sodium intake. It seemed of interest, therefore, to determine whether the mechanisms underlying the dissimilar actions of these two groups of steroids would be reflected in the electrolyte composition of the tissues of animals given one or the other compound under conditions of sodium loading as well as of sodium restriction. A preliminary study analyzing pooled samples of tissue indicated that the hypertension induced by DCA was accompanied by an increase in carcass sodium, whereas this did not obtain in the carcasses of rats made hypertensive with cortisone (5).