Inactivation of posterior pituitary antidiuretic hormone of the liver.

It has long been recognized that the liver bears some important relation to water metabolism (reviewed by Pick, 1929 and 1946; Ratnoff and Patek, 1942). In experimental liver damage (Adlersberg, 1934; Adlersberg and Fox, 1943) and in liver disease of man (Labby and Hoagland, 1947; Ralli et al., 1945; Leslie et al., 1948) water retention has been reported. The presence of antidiuretic substances in urine has been associated with liver dysfunction (Ralli et al., 1945; Leslie and Ralli, 1947; Hall, Frame and Drill, 1949). The suggestion has been made that this may be the well known neurohypophyseal antidiuretic hormone (ADH) appearing in the urine because it is not effectively inactivated by the damaged liver (Ralli et al. 1945). ADH is inactivated at some body site as judged by the small amounts excreted after injection (Heller and Urban, 1935; Ingram, Ladd and Benlbow, 1939) and the in vitro studies of Heller and Urban (1935) indicate that while kidney and blood inactivate ADH, liver tissue is more effective.