Metabolism of salt-retaining hormone by surviving liver slices

Evidence has been produced in this and other laboratories that the impaired capacity to excrete sodium which characterizes a number of clinical states involving edema, ascites and anasarca, is mediated, in part at least, through a humoral fac-tor emanating, in all probability, from the adrenal cortex (1-8). It now appears almost certain, on the basis of available evidence, that this substance, generally referred to in this paper as salt-retaining hormone or electrocortin, is aldosterone or a de-rivative of it (9, 10). Since quantitative measurements indicate that this sodium-retaining hormone is excreted in the urine in abnormally high concentration under these pathological conditions, curiosity concerning the underlying mechanism naturally arises. Two hypothetical possibilities are suggested: 1. Over-production of salt-retaining hormone by the adrenal cortex initiates an abnormal anti-natri-uretic and antidiuretic response. 2. Physiological inactivation or metabolism of the hormone by ex-tra-adrenal tissues is impaired with a resulting rise in blood, tissue and urine concentrations of "active " hormone. However, it is possible that accumulation of salt-retaining hormone, whatever its cause, bears no cause and effect relationship to fluid retention and other related manifestations of disease. In view of the recent evidence by Conn (11, 12) and Mader and Iseri (13) consideration must be given to the first of these possibilities. "Primary aldosteronism, " a new syndrome described by these investigators, is characterized by hyperna-' This work has been supported in part by funds pro-vitded by the Smith, Kline and French Laboratories of Pniiiadelphia, and also by grants from the Wisconsi