It has been previously shown that rats subjected to obstructive cholestasis demonstrate in the postcholestatic period, after release of common duct obstruction, a marked increase in canalicular bile flow relative to bile acid excretion. To characterize this phenomenon further, we investigated whether changes in canalicular permeability and in the activity of (Na+-K+)-ATPase in isolated liver surface membranes are associated with postcholestatic choleresis. With this purpose, the clearances of 14C-erythritol and 3H-insulin were simultaneously measured in rats subjected to a 3-day obstructive cholestasis and in controls, during spontaneous choleresis as well as during the intravenous infusion of sodium taurocholate at both submaximal and saturating rates. In additional groups of bile duct-ligated rats and controls, liver surface membrane fractions were isolated, and the activity of appropriate marker enzymes and (Na+-K+)-ATPase was determined. In both groups 14C-erythritol clearance closely approximated total bile flow, suggesting that bile flow was of canalicular origin. However, cholestatic rats showed a sixfold increase in 3H-inulin clearance compared to controls. These results suggest that canalicular permeability to inulin is markedly increased in cholestatic rats. On the other hand, (Na+-K+)-ATPase activity was significantly higher in cholestatic rats than in controls in both homogenate (1.27 +/- 0.07 and 0.89 +/- 0.07 U/mg of protein, respectively, p less than 0.001) and liver surface membranes (22.6 +/- 1.2 and 17.5 +/- 1.2 U/mg of protein, respectively, p less than 0.001). Thus enhanced choleretic response to bile acids in the postcholestatic period is associated with an increased permeability of canalicular structure to inulin and with a significant increase in both homogenate and surface membrane (Na+-K+)-ATPase activity. In addition, this study points out some important differences between bile secretory function of rats subjected to obstructive cholestasis and that described in models of bile secretory failure induced by drugs or monohydroxy-bile acids.