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 ac id taurocholate (TC) was assessed using isolated rat hepatocytes. Na+- dependent TC cotransport was determined in hepatocytes from female non pregnant, pregnant (19-20 days pregnant), postpartum (48 hr postpartum ) and postpartum rats treated with bromocriptine to block PRL secretio n. In separate experiments ovariectomized rats were infused i.v. with solvent alone (OVX) or with ovine PRL (100, 300 and 600 mug/day) for 7 days (OVX + oPRL). The least squares estimates of K(m) (muM) and V(ma x) (nmol/min/mg protein) for Na+-dependent TC uptake were, respectivel y: 15 and 1 in nonpregnant, 9 and 0.4 in pregnant, 9 and 1.1 in postpa rtum and 15 and 1 in bromocriptine-treated postpartum rats, and were 1 5 and 1 in OVX, 15 and 1 in OVX + oPRL (100 mug/day), 30 and 2 in OVX + oPRL (300 mug/day) and 18 and 2 in OVX + oPRL (600 mug/day) rats, re spectively. Calculation of the 95% joint confidence limits for K(m) an d V(max) showed that Na+-dependent TC uptake was significantly decreas ed in pregnant rats, and significantly increased in postpartum rats re lative to nonpregnant controls. Bromocriptine-treated postpartum rats were not different from controls. Infusion of 300 and 600 mug/day oPRL significantly increased Na+-dependent TC transport relative to OVX ra ts. Na+-K+-ATPase activity did not differ among the groups. These data indicate that PRL is responsible for the increased Na+-dependent tran sport of TC in the maternal liver postpartum, and that administration of oPRL to ovariectomized rats increases this transport in a dose-depe ndent manner.