The ability of urine extracts to inhibit sodium and potmdum-activated ATPaee, cross-react with antidigorin antibodies and induce natriureaie in rats was investigated in 10 healthy subjects, 10 cirrhotic patients without aecites (compensated cirrhotics), 27 nonacotemic cirrhotic patients with ascites and 10 cirrhotic patients with aecitem and functional renal failure to aeeeee whether reduced activity of natriuretic hormone contributes to sodium retention in cirrhosis. No ei-cant differencem were seen between healthy subjecte and compensated cirrhotic patients in any of these parametera (80dium and potaeeium-activated A T P m inhibition = 178.5 f 19.8 w. 247.4 f 48.7 nmol equivalent of ouab a i n / w digodnlb activity = 43.9 f 6.1 w. 48.0 f 5.6 ng equivalent of digoxidda~ natiuretic activity = 0.36 f 0.15 w. 0.63 f 0.27 pmoUmin). Cirrhotic patients with aecitem with and without functional renal failure showed signiilcantly higher values of sodium and potaseium-activated ATPam inhibition (708.1 f 94.0 and 529.2 f53.9 nmol equivalent of ouabainlday, reepectively), digoxinlike activity (138.9 * 7.2 and 116.3 * 7.9 ng equivalent of digoxidday) and natiuretic activity (1.78 f 0.48 and 1.93 f 0.37 pmoUmin) than healthy subjects and compensated cirrhotic patients. W e saw no significant differetmea between these two groups of cirrhotic patients with aedtes with respect to these parametem. In the drrhotic patients studied, sodium and potmiumactivated ATPaee inhibition and antidigorin antibodies directly correlated with the detgme of impairment of hepatic and renal function, plasma renin