M.: Regulation of bile salt transport in rat liver: Evidence that increased maximum bile salt secretory capacity is due to increased cholic acid receptors

rats increases maximum excretory capacity for tau-rocholate. We examined whether increased bile salt transport is due to recruitment of centrolobular trans-port units or rather to adaptive changes in the hepa-tocyte. Daily sodium cholate (100 mg/100 g body wt) was administered orally to rats. This treatment was well tolerated for at least 4 d and produced an 8.2-fold expansion of the bile salt pool. This expanded pool consisted predominently (99%) of cholic and deoxy-cholic acids. Significantly increased bile salt transport was not observed until 16 h after bile acid loading, and maximum elevations of transport capacity to 2.3-fold of control required-2 d. In contrast, maximum sul-fobromophthalein excretion rates increased 2.2-fold as early as 4 h and actually fell to 1.5-fold increase at 4 d. We studied the possibility that this adaptive increase in bile salt secretory transport was due to changes in canalicular surface membrane area, lipid composition, or increased number of putative carriers. Canalicular membrane protein recovery and the specific activities of leucine aminopeptidase, Mg++-ATPase and 5'-nu-cleotidase activities were unaltered by bile salt pool expansion. The content of free and esterified choles-terol and total phospholipids was unchanged in liver surface membrane fractions compared with control values. In contrast, sodium cholate administration se