Comparative fates of intravenously and orally administered aldosterone: evidence for extrahepatic formation of acid-hydrolyzable conjugate in man.

Abstract

It is well established that the liver is a major site of metabolic inactivation of aldosterone. In 1962 Coppage, Island, Cooner, and Liddle (2) reported that the human liver was capable of con- verting aldosterone both to its acid-hydrolyzable conjugate (AHC) 1 and to tetrahydroaldosterone. The same study also demonstrated that aldosterone was almost completely inactivated during a single passage through the normal liver. More recent studies by Luetscher and associates (4) have indi- cated that the normal liver extracts about 97%o of the aldosterone delivered to it by the arterial circulation, and the studies of Bougas and co-work- ers (5, 6) have indicated that in subjects with minimal cardiac dysfunction the rate of splanchnic clearance of aldosterone amounts to about 89%o of the hepatic blood flow.