Mean plasma levels of hANF at admission were significantly higher in liver cirrhosis (LC) patients with ascites (93 +/- 11 ng, n = 20; p less than 0.05) than in LC-patients without ascites (32 +/- 14 ng/l, n = 11) or healthy controls (31 +/- 15 ng/l; range: 5-80 ng/l; n = 106). Diuretic treatment of patients with LC and ascites normalised hANF plasma concentrations (44 +/- 14 ng/l; p less than 0.05). Increase of plasma hANF in LC-patients with ascites after acute volume expansion was lower (relative rise: 159%) than in those without ascites (relative rise: 223%). Volume redistribution into the vascular compartment, induced by peritoneovenous shunt implantation in LC-patients with diuretic treatment-refractory ascites, resulted in a sharp increase of plasma hANF levels (344 +/- 87 ng/l = 420% of preoperative concentration). Normal and slightly increased levels of plasma hANF and the appropriate regulation to volume changes suggest an intact control of the hormone in LC-patients. Neither a lack nor an inappropriate secretion of hANF as a cause for sodium retention as postulated by the overflow theory of ascites accumulation could be found in liver cirrhosis.