Prolactin increases Na+/taurocholate cotransport in isolated hepatocytes from postpartum rats and ovariectomized rats.

The role of prolactin (PRL) in regulating the transport of the bile acid taurocholate (TC) was assessed using isolated rat hepatocytes. Na(+)-dependent TC cotransport was determined in hepatocytes from female nonpregnant, pregnant (19-20 days pregnant), postpartum (48 hr postpartum) and postpartum rats treated with bromocriptine to block PRL secretion. In separate experiments ovariectomized rats were infused i.v. with solvent alone (OVX) or with ovine PRL (100, 300 and 600 micrograms/day) for 7 days (OVX+oPRL). The least squares estimates of Km (microM) and Vmax (nmol/min/mg protein) for Na(+)-dependent TC uptake were, respectively: 15 and 1 in nonpregnant, 9 and 0.4 in pregnant, 9 and 1.1 in postpartum and 15 and 1 in bromocriptine-treated postpartum rats, and were 15 and 1 in OVX, 15 and 1 in OVX+oPRL (100 micrograms/day), 30 and 2 in OVX+oPRL (300 micrograms/day) and 18 and 2 in OVX+oPRL (600 micrograms/day) rats, respectively. Calculation of the 95% joint confidence limits for Km and Vmax showed that Na(+)-dependent TC uptake was significantly decreased in pregnant rats, and significantly increased in postpartum rats relative to nonpregnant controls. Bromocriptine-treated postpartum rats were not different from controls. Infusion of 300 and 600 micrograms/day oPRL significantly increased Na(+)-dependent TC transport relative to OVX rats. Na(+)-K(+)-ATPase activity did not differ among the groups. These data indicate that PRL is responsible for the increased Na(+)-dependent transport of TC in the maternal liver postpartum, and that administration of oPRL to ovariectomized rats increases this transport in a dose-dependent manner.