METABOLISM OF SALT-RETAINING HORMONE BY SURVIVING LIVER SLICES 1

Abstract

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).