In vitro investigation demonstrates hepatic metabolism of the adrenal hormone aldosterone, suggesting a key clearance pathway for controlling sodium retention.
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).
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Chart et al. (1956) studied this question.
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