The evocation of hypertensive cardiovascular renal disease in experimental animals through desoxycorticosterone administration suggests that essential hypertension and its sequellae may be the result of increased activity by endogenous salt-retaining corticosteroids. Such a possibility does not necessarily imply greater production of cortical substances but might represent a defect in removal. Detoxification of gonadal steroids is accomplished in the liver (Engel, 1944; Kochakian, Haskins and Bruce, 1944; Krichesky, Benjamin and Slater, 1943). The experimental data relative to the adrenal steroids are somewhat equivocal. The inactivity of desoxycorticosterone when orally administered (Kuizenga, Nelson and Cartland, 1940), its chemical similarity to progesterone and the identity of at least one of the detoxification products of both substances (Hoffman, Kazmin and Browne, 1943) suggest a common metabolic pathway through the liver. This supposition is supported by the decreased growth and survival rates of adrenalectomized animals when desoxycorticosterone pellets are implanted in the mesentery or spleen rather than in the subcutaneous tissues (Eversole and Gaunt, 1943).